Gene therapy for hearing loss and vestibular disorders

Abstract

Provided are recombinant nucleic acids and vectors including a TOMT regulatory element, pharmaceutical compositions including the recombinant nucleic acids and vectors, and methods of use thereof.

Description

[0001]8123-110315-03GENE THERAPY FOR HEARING LOSS AND VESTIBULAR DISORDERS CROSS REFERENCE TO RELATED APPLICATIONS This claims the benefit of U.S. Provisional Application No.63 / 544,914, filed October 19, 2023, and U.S. Provisional Application No.63 / 662,079, filed June 20, 2024, both of which are incorporated herein by reference in their entireties. FIELD The disclosure relates to compositions and methods for gene therapy, particularly gene therapy for the treatment of hearing loss and / or vestibular disorders. ACKNOWLEDGMENT OF GOVERNMENT SUPPORT This invention was made with government support under grant nos. R21-DC019195, R01- DC019618, R01-EB033172 awarded by the National Institutes of Health. The government has certain rights in the invention. INCORPORATION OF ELECTRONIC SEQUENCE LISTING The Sequence Listing is submitted as an XML file named “Sequence.xml,” created on October 17, 2024, 27,709 bytes, which is herein incorporated by reference in its entirety. BACKGROUND Hearing loss is one of the most prevalent sensory deficits, yet there are no biological therapies. In addition, genetic mutations that cause hearing loss often also cause vestibular disorders. Hereditary (genetic) forms of hearing loss occur in 50-80% of individuals born with hearing loss, thus gene therapy is an attractive treatment strategy. However, currently available viral vectors for cochlear gene therapy utilize ubiquitous promoters (e.g., CMV, CAG, etc) or other promoters (e.g. MYO15), which express genes at abnormally high levels, infect many different cell types (target cell types and non-target cell types), and / or cause toxicity to hair cells. For these reasons, hearing rescue with currently available vectors has been limited to partial restoration of function with variable durability. Thus, improved materials and vectors for gene therapy to treat hearing loss and / or vestibular disorders are needed. SUMMARY Disclosed are recombinant nucleic acid molecules comprising a transmembrane-O- methyltransferase (TOMT) regulatory element operably linked to a nucleic acid molecule. In some examples, the regulatory element is a promoter or enhancer. The TOMT regulatory element drives expression of operably linked nucleic acids in hair cells of the cochlea and / or vestibule. In some examples, the TOMT regulatory element is a human or murine TOMT promoter and / or enhancer. In some examples, the nucleic acid operably linked to the TOMT regulatory element is a gene associated with hearing loss8123-110315-03and / or vestibular disorders, for example, a TOMT gene (e.g., a human TOMT gene). In some examples, the nucleic acid comprises the coding sequence (CDS) or cDNA of a gene associated with hearing loss and / or vestibular disorders. Also disclosed are vectors including a recombinant nucleic acid molecule disclosed herein. In some examples, the vector is an adeno-associated virus (AAV) vector. Also included are host cells transformed with a recombinant nucleic acid or vector disclosed herein; and methods of producing a heterologous protein in a host cell, including transforming the host cell with a recombinant nucleic acid or vector disclosed herein. Further disclosed are pharmaceutical compositions including a recombinant nucleic acid or vector disclosed herein. The pharmaceutical compositions are useful for treating hearing loss, such as genetic hearing loss, and / or vestibular disorders. Also disclosed are methods of treating hearing loss and / or vestibular disorders in a mammalian subject including administering an effective amount of a pharmaceutical composition disclosed herein to the subject. A subject having hearing loss (e.g., genetic hearing loss) and / or vestibular disorder can be selected for treatment. In some examples, administering the pharmaceutical composition induces expression of a hearing loss and / or vestibular disorder associated gene (e.g., TOMT) in cochlear and / or vestibular hair cells of the subject. In some examples, administering the pharmaceutical composition induces expression of a hearing loss associated gene (e.g., TOMT) in cochlear hair cells of the subject The foregoing and other objects and features of the disclosure will become more apparent from the following detailed description, which proceeds with reference to the accompanying figures. BRIEF DESCRIPTION OF THE DRAWINGS FIGS.1A-1I show that TOMT is specifically expressed in prehearing and adult hair cells. FIGS. 1A-1B are RNAscope® (a multiplex nucleic acid in situ hybridization technique) cryosections from postnatal day (P)7 cochlea to examine mRNA expression. FIG.1A shows that Tomt mRNA is restricted to inner hair cells (IHCs) and outer hair cells (OHCs); Myo7a mRNA is expressed by hair cells and some support cells. FIG.1A includes DAPI staining to label all cell nuclei. FIG.1B shows Tomt mRNA is expressed in cochlear IHCs and OHCs from an 8-week-old adult mouse. FIGS.1C-1I show HA-tagged TOMT protein immunolabeling in cryosections and whole mounts (WM) from TOMT-HA knock-in mice. FIG.1C shows that TOMT is expressed solely by cochlear and vestibular hair cells in a P7 cryosection. FIG.1C includes DAPI staining. FIG.1D shows that TOMT is expressed exclusively by hair cells throughout the cochlear spiral. Data are from a P0 mouse WM. FIG.1E shows TOMT is distributed throughout the cell body and excluded from stereocilia. Image from a P10 mouse WM. Phalloidin to label hair cell stereocilia is shown. FIG.1F shows TOMT expression in E16.5 hair cells, labeled with MYO7A. FIG.1G shows TOMT expression in P7 hair cells labeled with MYO7A FIG.1H shows TOMT-HA expression in adult hair cells. FIG.1H includes phalloidin to label stereocilia and calretinin staining to label hair cells. FIG.1I shows TOMT colocalizes with a marker for the endoplasmic reticulum (ER-mOXGFP) from a P8 cochlear WM.8123-110315-03FIG.2 shows a schematic depicting the mouse Tomt genomic locus (chromosome 7:101,898,200- 101,907,299) for both transcript variants (TV1 and TV2), and the relative locations of Tomt promoter fragments described herein. Tomt TV2 exon 1 CAGEATAC (Tomt TV2 CAGEATAC) and Tomt TV2 exon 1 CAGE (Tomt TV2 exon 1 CAGE) fragments are smaller truncations of TOMT TV2 exon 1. Exons are numbered above; coding sequence exons are filled boxes while untranslated exons are open boxes. FIGS.3A-3F show that the Tomt TV2 Exon 1 promoter drives hair cell-type-specific expression in the cochlea. In FIGS.3A-3D, whole mount cochlea from postnatal day (P)7 mice were injected at P2 with adeno-associated viral (AAV) vectors (serotype PHP.eB) containing a novel gene regulatory fragment from the Tomt genomic locus (Tomt TV2 exon 1 fragment) driving GFP expression or ubiquitous CAG promoter driving expression of TdTomato. FIGS.3A-3C show low magnification images of cochlear whole mounts demonstrating expression driven by Tomt TV2 exon 1 fragment vs. CAG promoter. Individual channels are at middle (TV2-GFP) and right (CAG-TdTomato). Viral expression of Tomt-TV2-GFP is highly restricted to hair cells throughout the apical-to-basal extent of the cochlea, with a few scattered additional cell types. In contrast, CAG-tdTomato is expressed by a much broader population of cochlear cells (hair cells, support cells, etc). FIG.3D shows high magnification images of a cochlear whole mount demonstrating expression driven by Tomt TV2 exon 1 fragment vs. CAG promoter in hair cells. Individual channels are at middle (TV2-GFP) and right (CAG-TdTomato). Inner and outer hair cells express TV2-GFP exclusively, while CAG-TdTomato is expressed by many other support cells (white arrowheads) in addition to hair cells. FIGS.3E-3F show whole mount cochleae from P8 mice injected at P1 with AAVs (serotype PHP.eB) containing the Tomt TV2 exon 1 fragment driving GFP expression (FIG.3E) or the ubiquitous CMV promoter driving GFP expression (FIG.3F). Tissue was immunostained for the hair cell marker MYO7A and a nuclei marker (DAPI). GFP expression driven by the Tomt TV2 exon 1 fragment is highly restricted to hair cells (MYO7A+ cells) throughout the apical-to-basal extent of the cochlea, with a few scattered additional cells. In contrast, GFP driven by the CMV promoter is expressed by a much broader population of cochlear cells. Scale bar = 100 μm. FIGS.4A-4B show that the Tomt TV2 exon 1 CAGEATAC genomic fragment drives selective expression in cochlear hair cells. FIG.4A show whole mount cochleae from P8 mice injected at P1 with AAVs (serotype PHP.eB) containing the TOMT TV2 exon 1 CAGEATAC fragment driving GFP expression. Tissue was immunostained for the hair cell marker MYO7A (B) and a nuclei marker (DAPI). GFP expression driven by the Tomt TV2 exon 1 CAGEATAC fragment is highly restricted to hair cells throughout the apical-to-basal extent of the cochlea, with some scattered additional nonsensory cells. Individual GFP channel is on the right; scale bar = 200 μm. FIG.4B shows a high magnification image of a cochlear whole mount demonstrating expression driven by Tomt TV2 exon 1 fragment. Individual GFP channel is on the right. Nearly 100% of hair cells express CAGEATAC-GFP exclusively, while support cells do not. FIGS.4C-4D show that Tomt promoters are highly specific for hair cells. Quantification of the proportion of GFP+ cells driven by commonly used promoters (FIG.4C) and novel Tomt promoters (FIG.8123-110315-034D) that are co-labeled with MYO7A+ hair cells in cochlear whole mounts at P28. Injections of AAV- PhP.eB-GFP, with various promoters, were performed at P1-P3.4 weeks later, cochleas were dissected, fixed and immunostained for MYO7A. GFP+ / MYO7A+ double positive cells were compared to the total number of GFP+ cells. Data represent averages across n=3 injected animals. FIGS.4E-4I show ubiquitous and Myo15 promoters are expressed by many spiral ganglion neurons (SGNs) in the cochlea, while Tomt promoters (fragments) are expressed by very few. Cochlear cryosections immunostained for TUJ1 to label spiral ganglion neurons from P28 mice injected between P1-P3 with AAVs (serotype PhP.eB) expressing GFP driven by various promoters. On the left is a merged image, middle image is GFP fluorescence as a measure of promoter activity, and right graph is quantification of the proportion of TuJ1+ SGNs that are GFP+ from the apex, middle, and basal regions of the cochlea. (FIG. 4E) CMV promoter; (FIG.4F) CAG promoter; (FIG.4G) Myo15 promoter; (FIG.4H) Tomt TV2 exon 1 promoter; (FIG.4I) Tomt TV2 exon 1 CAGEATAC promoter. A few GFP+ SGNs for Tomt (FIGS.4H-4I) promoters have much lower levels of fluorescence. Data are minimum of n=3 biological replicates (animals). Scale bar in 4E = 50 um, applies to all panels. FIG.5 shows inner ear AAV-mediated delivery of TOMT with Tomt TV2 exon 1 CAGEATAC rescues hearing in Tomt mutant mice (as measured by auditory brainstem response (ABR)) more efficiently than other tested promoters used for hearing loss gene therapy. Click and pure tone ABR thresholds for 4- week-old Tomt + / - untreated (n=3), Tomt - / - untreated (n=4, purple) and Tomt - / - injected mice at P1-P2 with AAV-TOMT (serotype PhP.eB) driven by the CMV promoter (n=4), Myo151 kb fragment (promoter) (n=5), Tomt TV2 exon 1 fragment (n=9), or Tomt TV2 exon 1 CAGEATAC fragment (n=4). Data are mean±SEM, *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001, ns, not significant (ANOVA followed by multiple comparisons test relative to Tomt + / - untreated). Arrows indicate that although 90 dB is the upper limit of our testing for ABR, thresholds are likely much higher. FIG.6 shows inner ear AAV-mediated TOMT expression in wildtype mice. TOMT expression by Tomt TV2 exon 1 fragment or Tomt TV2 exon 1 CAGEATAC fragment does not affect hearing, while TOMT expression by either Myo151 kb fragment or CMV promoter causes significant hearing loss. Click and pure tone ABR thresholds (decibels, dB) for 4-8 week-old C57BL6J untreated (n=3), saline (n=3) or injected at P1-P2 with AAV-PhP.eB-Tomt TV2 exon 1 fragment-TOMT (n=6), AAV-PhP.eB-Tomt TV2 exon 1 fragment CAGEATAC-TOMT (n=3), AAV-PhP.eB-Myo151 kb-TOMT (n=3), AAV-PhP.eB-CMV- TOMT (n=3) or Saline (n=3). Data are mean±SEM, *p<0.05, **p<0.01, ****p<0.0001, n.s. not significant (ANOVA followed by multiple comparisons test relative to Tomt + / - untreated). FIGS.7A-7C show expression patterns of additional tested Tomt promoter fragments. Whole mount cochlea from postnatal day (P)7 mice injected at P2 with adeno-associated viral (AAV) vectors (serotype PHP.eB) containing fragments from the Tomt genomic locus driving TOMT-HA expression are shown. Individual channels are at middle (Tomt fragment driving expression of TOMT-HA) and right (MYO7A to mark hair cells, DAPI to label nuclei). FIG.7A shows that Tomt TV1 exon 1 fragment drives broad expression in many cell types including hair cells, support cells and neurons. FIG.7B shows that Tomt TV18123-110315-03and TV2 exon 1 fragment does not exhibit significant promoter activity. The weak fluorescence that is shown is tissue autofluorescence. FIG.7C shows that Tomt TV1 and TV2 exon 2 has some activity in hair cells, along with other scattered cochlear cells. Scale bar in A = 100 mm. FIGS.8A-8F show that CMV and Myo15 promoters driving TOMT expression cause significant hair cell death in wildtype mice. Whole mount images of adult (P28) mice immunostained for MYO7A and uninjected (FIG.8A) or injected at P1-3 with saline (FIG.8B); AAV-PhP.eB-CMV promoter-TOMT-T2A- eGFP (FIG.8C), AAV-PhP.eB-Myo15 promoter-TOMT-T2A-eGFP (FIG.8D), AAV-PhP.eB-Tomt TV2 exon 1 promoter-TOMT-T2A-eGFP (FIG.8E), or AAV-PhP.eB-Tomt TV2 exon 1 CAGEATAC promoter- TOMT-T2A-eGFP (FIG.8F). Note significant loss of inner hair cells (IHCs) and outer hair cells (OHCs) with CMV promoter, loss of IHCs with Myo15 promoter, while whole mounts from mice injected with Tomt promoter fragments appear similar to those uninjected and saline-injected with no apparent hair cell loss. White arrowheads point to missing IHCs and yellow asterisks indicate missing OHCs. FIGS.9A-9D show that AAV-mediated delivery of TOMT rescues vestibular function in Tomt mutant mice. (FIG.9A) Gene therapies (AAV.PHP.eB-TOMT-P2A-eGFP, with various promoters) are delivered to the posterior semicircular canal of neonatal (postnatal day 1-3) wild-type and Tomt (- / -) mutant mice.4 weeks later, vestibular function is assessed with open field test. (FIG.9B) Representative traces from open field tests for wildtype (left), untreated Tomt mutant mice (middle), and Tomt mutant mouse treated with 4 weeks after treatment. (FIG.9C) Tomt mutant mice have vestibular deficits. Distance traveled (cm) by 4-week-old Tomt + / - (n=8) and Tomt - / - (n=8) mice in 60 mins with Open Field Test. Data are mean ± SEM. *, p<0.05; **, p<0.01; ***, p<0.001; ****, p<0.0001. (FIG.9D) AAV-mediated inner ear delivery of Tomt with various promoters rescues vestibular (circling) deficits in Tomt mutant (Tomt- / - treated) mice. Qualitative assessment of rescue for various promoters. Most mice exhibit normal vestibular behavior (no circling or head tilting) after rescue. Each number represents one injected mouse, evaluated 4 weeks after treatment. SEQUENCES The nucleic acid and amino acid sequences listed herein are shown using standard letter abbreviations for nucleotide bases, and single letter code for amino acids. Only one strand of each nucleic acid sequence is shown, but the complementary strand is understood as included by any reference to the displayed strand. SEQ ID NO: 1 Mouse Tomt TV2 Exon 1 promoter fragment. ATATTTATTGTCTATAGTGTGCCACTCTAGTGTTCAGTTTGGATAGGTAGCTGGGCAGAAAACA GCCCAAGATCCAGACCATGGAATCCCTAGTCAGGTGGTCAGTGTATTCTATAGTTGTGTTTTTT AGTTCATTTCTTCTACCACATGTGAGTAACTGAGAGACAAGGACAGAGTCTGACTTTACTCTGT AACTGATACCCTAACACTTACTTACAGAAAACTTGGGGAGCTGGGCATGGTGGCGCAGGCCTT TAATCCCAGCACTTGGGAGGCAGAGGCAGGCGGATTTCTGAGTTCGAGGCCAGCCTGGTCTAT AAAATGAGTTCCAAGACAGCCAGGGCTATAGAGAGAAACCCTGTCTCAAAAAACAAAACAAA CAAACAAACAACCCAGAAAACTTGGGTTTTGAATTCAGTAAATAATTTTCAATTACTTTGGTTT ACACCATGCCGCATGTCCTGATCCCAAGGGGTTAGAAAAGTCACCTAGTAATATTTATTAATTC8123-110315-03TTCAGATTAAGACCCTAGAGTTCTGCTAAGTTTCTCAAAGGCCTGAGAAATAGGAGGCAGCTG AAGTTTGGTAACCTGAACTGCAGGTCTCAGGTAACAACAGCCTCAACATCAATAATTGAAATC AGGTCCAGCCTCCATCCTTGGGGTTAGTCCTCTGAAGGACTCCCATTCCGGTACCTGGTCTTTCT TAGGAGCCTTCAGCTCAGGTAAGCAGGGCCTTGTGGGTTCTCAGGTACATCAATTCATGCCCAC ATCACAAATGCTTCACATTCCTTCATACAATCTAGATTTTAACAGACACCCCTCTTCCAACCAA GGGTCTTGCAAAAATAGCCTATCAGGCTCCGATCTAAGGGGAGGAGCAGGGGGGGAAAGAAC AGCTATCCCCTATAGGTGGTCCTGGAGAAGAAAGCTGAATGGTGAGAATGTGTGGTGTGTGCA TGTACATATTTGCACTTACAGAGAATTCTCTTTGGAGGGGGATACAAATATAAAAATACAGGA CTGGAGAAAATACACAGGACCAGGGAGGACCCACACCTCCAGGGAAGAGCAAACAGAAAATC CTTGGATAGAAAAAACAAACACTCCACTCTAACATGGTAT SEQ ID NO: 2 Mouse Tomt TV1 and TV2 Exon1 promoter fragment. CTCCACTAGACCGGGTGAAACTGTTCTCTGTGGCACGGTGCCTACTGTGTGTAGACATCAGGGC TCAGGCTTCGAGGCAGCTGTTAAGAGGAATGGCCAGGGGGCTGACACCCAGCCTTGCAAAAGT CTTCCCCTCCTCAAAAGCGTCTAGGCAGGGAAGGGACTGTAGTAGAGAGGAATGAGATGCACC AAGGGGAAGATGGAAATTTAAAAACAAGACACTGAAGTCTCTCCAAGTCGATGCTTTCTCGAA AAGAGTAAGATCTACAATCACATTCTTCAGAGAGGAACTCTCTAGCTCGAGGAACCCTCAGGC ACCAGGCAGGGAACAGCAAACCAAACTCATAAATCAAATCCCCTTTCCTCTATATCGGTCAAA GCAAACTCTATTGCTCCCCAACGTCCCGATGTCTTCGCTCTATTAATTCTTCACTGGCCAACTCA AATGACAGTAACTTGGTGTCAACTTTTGACACCAAGCCAACAGTGGCAGAACAGTTGACAGAA CACACAGAAATTCCTGATTTATCTCGGGAGACTGAGAGCCTCAAATTACCTATCTCTACAATGG GTCCACTAAGCCAAGCTGCAGTGAAGACAGAGGAATCTGTGAGCGCGAATGTTTCCCGAGAAC CCAGTCTGAGGATTCGAGTGGTGAGATACGAGGGGACTGGAGAGTGGAAGGGGAGGGGCCGA GTCAGGCGGCGACCGCCGCAACCCTAGGCAGAAGTAAGACTAGGATCTTTAAGAGGGTAGGA GCCCGGCTGGCCGTCCTCTCTGTAATCTGTCCCCTCCAGGCCTCCGTACTCGGTGAGCCTGCAG TCCGGCTCCCCGCCACTGCGGGCTTTATTCTGGGCCCCGAGCCCCGCGGTCGTAGCCCACAGTC CCAAACCCCGTCCGCCGCTGTCGCACCTGGTCCGAGTCCTCGTTTTCGCTGCTATAGCAGCACC CCATGGCGGGGTCGGGCCGGGCGCTCAGGCGGCGCCGAGGAGGGACGGCGTCCGTCAGGAGC CTTTCCGGTCACATGACCCGCGGCTGCCTCTCGCTCCCCTCCCCCTCGCCTAGCCTGTCCTAAAG CCGCTCCGGCGCCACAGCCAAATCTTGCCTTCCGGTCCCGCCTCGCCGCGTGACAATCGCCAAC CAATGGAAAAGTGCGTCCTACGTGAGCGGACCCGCGGCACGTGATAGGAAGGCAGGCGGGGC GAGTCACATGATTTTGTTGTCCTAGTCTCTAACTCCGAATCCTTGCGTCCCTTAGCTTTAGTGGC CAGTGCAGTGCGACGAGTTGTGTGGTCACATGGTGTCAGGGCCACCTTTGTGGGCCCAGTGCTA TATCAAGATAAATTCTTAAGTGCCATGCATATTTATTGTCTATAGTGTGCCACTCTAGTGTTCAG TTTGGATAGGTAGCTGGGCAGAAAACAGCCCAAGATCCAGACCATGGAATCCCTAGTCAGGTG GTCAGTGTATTCTATAGTTGTGTTTTTTAGTTCATTTCTTCTACCACATGTGAGTAACTGAGAGA CAAGGACAGAGTCTGACTTTACTCTGTAACTGATACCCTAACACTTACTTACAGAAAACTTGGG GAGCTGGGCATGGTGGCGCAGGCCTTTAATCCCAGCACTTGGGAGGCAGAGGCAGGCGGATTT CTGAGTTCGAGGCCAGCCTGGTCTATAAAATGAGTTCCAAGACAGCCAGGGCTATAGAGAGAA ACCCTGTCTCAAAAAACAAAACAAACAAACAAACAACCCAGAAAACTTGGGTTTTGAATTCAG TAAATAATTTTCAATTACTTTGGTTTACACCATGCCGCATGTCCTGATCCCAAGGGGTTAGAAA AGTCACCTAGTAATATTTATTAATTCTTCAGATTAAGACCCTAGAGTTCTGCTAAGTTTCTCAAA GGCCTGAGAAATAGGAGGCAGCTGAAGTTTGGTAACCTGAACTGCAGGTCTCAGGTAACAACA GCCTCAACATCAATAATTGAAATCAGGTCCAGCCTCCATCCTTGGGGTTAGTCCTCTGAAGGAC TCCCATTCCGGTACCTGGTCTTTCTTAGGAGCCTTCAGCTCAGGTAAGCAGGGCCTTGTGGGTT CTCAGGTACATCAATTCATGCCCACATCACAAATGCTTCACATTCCTTCATACAATCTAGATTTT AACAGACACCCCTCTTCCAACCAAGGGTCTTGCAAAAATAGCCTATCAGGCTCCGATCTAAGG GGAGGAGCAGGGGGGGAAAGAACAGCTATCCCCTATAGGTGGTCCTGGAGAAGAAAGCTGAA TGGTGAGAATGTGTGGTGTGTGCATGTACATATTTGCACTTACAGAGAATTCTCTTTGGAGGGG GATACAAATATAAAAATACAGGACTGGAGAAAATACACAGGACCAGGGAGGACCCACACCTC CAGGGAAGAGCAAACAGAAAATCCTTGGATAGAAAAAACAAACACTCCACTCTAACATGGTA T8123-110315-03SEQ ID NO: 3 Mouse Tomt TV1 and TV2 Exon 2 promoter fragment. TAGTGTTTTAAATTGCTTCTTACTGTGACAAAGTGCAGTGAGAATGTGAATGGGTTTCACAACA AAGCTGTTCTCTTTTGCTTCCCATAATGGATCAGAGGAGTCCAGGCAGACCAGGTATGGTAGGA GGAAGACACCCCAAGAAACAGATGAAAAAGGTCTTGAGGAAAGTCAGAAAGTGGGTGGGATC AGCAACAATGCAGTACTAGATCTGCAGCCAGGACCAGAGATATAGTTTGTGGTTGAGTGTTAA ACAGCAGGAGGTTGCAAAGAGCACAGGCTGAACTCAAATCCCAGTTCTGCTGTGTCTTTGGCA AAGGACAGCCTCTCAGACATGTTTGTATAAGCGTGGAAATTGCATAAATAAGTCTGCACAAAT GACAGGCAAATGGTACATCTAGGTTTCCCCGCCAGCCTCCCTCTATCCTAGGACCCAGGTAGGG ACAATGTCCCCTGCCATTGCACTGGCATTCCTGCCACTCGTGGTAACACTGCTGGTGAGATACC GGCACCATTTCCGACTGCTGGTGCGTACAGTCCTGCTGAGAGGATTTCGAGACTGCCTGTCAGG ACTTCGGATTGAGGAGCGGGCTTTCAGCTATGTGCTCACCCATGCCCTGCCTGGAGACCCTGGT CACATCCTCACCACGCTTGACCATTGGAGCAGCTGCTGCGAGTACCTGAGCCACATGGGCCCTG TTAAAGGTGAGTGTTCCTT SEQ ID NO: 4 Mouse Tomt TV1 Exon 1 promoter fragment. CTCCACTAGACCGGGTGAAACTGTTCTCTGTGGCACGGTGCCTACTGTGTGTAGACATCAGGGC TCAGGCTTCGAGGCAGCTGTTAAGAGGAATGGCCAGGGGGCTGACACCCAGCCTTGCAAAAGT CTTCCCCTCCTCAAAAGCGTCTAGGCAGGGAAGGGACTGTAGTAGAGAGGAATGAGATGCACC AAGGGGAAGATGGAAATTTAAAAACAAGACACTGAAGTCTCTCCAAGTCGATGCTTTCTCGAA AAGAGTAAGATCTACAATCACATTCTTCAGAGAGGAACTCTCTAGCTCGAGGAACCCTCAGGC ACCAGGCAGGGAACAGCAAACCAAACTCATAAATCAAATCCCCTTTCCTCTATATCGGTCAAA GCAAACTCTATTGCTCCCCAACGTCCCGATGTCTTCGCTCTATTAATTCTTCACTGGCCAACTCA AATGACAGTAACTTGGTGTCAACTTTTGACACCAAGCCAACAGTGGCAGAACAGTTGACAGAA CACACAGAAATTCCTGATTTATCTCGGGAGACTGAGAGCCTCAAATTACCTATCTCTACAATGG GTCCACTAAGCCAAGCTGCAGTGAAGACAGAGGAATCTGTGAGCGCGAATGTTTCCCGAGAAC CCAGTCTGAGGATTCGAGTGGTGAGATACGAGGGGACTGGAGAGTGGAAGGGGAGGGGCCGA GTCAGGCGGCGACCGCCGCAACCCTAGGCAGAAGTAAGACTAGGATCTTTAAGAGGGTAGGA GCCCGGCTGGCCGTCCTCTCTGTAATCTGTCCCCTCCAGGCCTCCGTACTCGGTGAGCCTGCAG TCCGGCTCCCCGCCACTGCGGGCTTTATTCTGGGCCCCGAGCCCCGCGGTCGTAGCCCACAGTC CCAAACCCCGTCCGCCGCTGTCGCACCTGGTCCGAGTCCTCGTTTTCGCTGCTATAGCAGCACC CCATGGCGGGGTCGGGCCGGGCGCTCAGGCGGCGCCGAGGAGGGACGGCGTCCGTCAGGAGC CTTTCCGGTCACATGACCCGCGGCTGCCTCTCGCTCCCCTCCCCCTCGCCTAGCCTGTCCTAAAG CCGCTCCGGCGCCACAGCCAAATCTTGCCTTCCGGTCCCGCCTCGCCGCGTGACAATCGCCAAC CAATGGAAAAGTGCGTCCTACGTGAGCGGACCCGCGGCACGTGATAGGAAGGCAGGCGGGGC GAGTCACATGATTTTGTTGTCCTAGTCTCTAACTCCGAATCCTTGCGTCCCTTAGCTTTAGTGGC CAGTGCAGTGCGACGAGTTGTGTGGTCACATGGTGTCAGGGCCACCTTTGTGGGCCCAGTGCTA TATCAAGATAAATTCTTAAGTGCCATGC SEQ ID NO: 5 Mouse Tomt TV2 exon 1 CAGE promoter fragment. TTGGGGTTAGTCCTCTGAAGGACTCCCATTCCGGTACCTGGTCTTTCTTAGGAGCCTTCAGCTCA GGTAAGCAGG SEQ ID NO: 6 Mouse Tomt TV2 exon 1 CAGEATAC promoter fragment. GAGGCAGGCGGATTTCTGAGTTCGAGGCCAGCCTGGTCTATAAAATGAGTTCCAAGACAGCCA GGGCTATAGAGAGAAACCCTGTCTCAAAAAACAAAACAAACAAACAAACAACCCAGAAAACT TGGGTTTTGAATTCAGTAAATAATTTTCAATTACTTTGGTTTACACCATGCCGCATGTCCTGATC CCAAGGGGTTAGAAAAGTCACCTAGTAATATTTATTAATTCTTCAGATTAAGACCCTAGAGTTC TGCTAAGTTTCTCAAAGGCCTGAGAAATAGGAGGCAGCTGAAGTTTGGTAACCTGAACTGCAG GTCTCAGGTAACAACAGCCTCAACATCAATAATTGAAATCAGGTCCAGCCTCCATCCTTGGGGT TAGTCCTCTGAAGGACTCCCATTCCGGTACCTGGTCTTTCTTAGGAGCCTTCAGCTCAGGTAAG CAGGGCCTTGTGGGTTCTCAGGTACATCAATTCATGCCCACATCACAAATGCTTCACATTCCTT CATACAATCTAGATTTT8123-110315-03SEQ ID NO: 7 An exemplary Human TOMT promoter fragment. ACACTGACCAGTCCAAGACAACGCGCGCCCCCACAAAGCACCTTCCCCGTCCCCATTTATGCCC AACCCATAAACCCAAAGTAGAGCCAACCTCGCACTGGCTACGTAACCCGGGCCAAGCTAAACA TTATAAACCTCAGGCTCCCCATCTTTAAAGTATAACAGGTGGTTAGAAGATTAAAAAGATAAA CATTTGGCAGGTCATTGTGGACGGTGTAGCTCAGAAAATGCTGACTACTGCACTACCATAACTA CTGCTATTGTTAACGATAAAAGGCAAAGACTTTCCAGGACCCGACCCCTCGCTTACAAGCCTTT CGGGAACTTGCCCTATACCCCCGACCCCAGTCACCTTCAGATTTAATTCCACAGACACGCCCCC AAACAGACCCTCCCCTTTAAGGCACCCCCCCCCCCCCCGGCTCCTCCCTCTCAGGCGCCTCTCC TCACAAACCTTACCCCCATAGATTCTGCCCTTTCGGACTCGGTTATGGAGGAGGCCTTCCGCTC GCAGCGGCCTCTCCAGCACCCCTTTTAGGCCTGAGCACCCGCAGGGGTGCCCAGGCCGCACGC CAAACGCGGGCCCGCGCCGGTTACCTGGCTGCGCGCTCCCGCTCTGCCTCGCGATTCTCCGGAA TCGTACCTCTTCGTGGGCTCGCGCCAGCGCTGTGAGCGCACAATTAGTTTAAACTATGGCCCCG CCCCCTCGCGCTGCCCTCTGATTGGCCTCTGTCGGCGGGGCCCGCTTAAGGACCCGGGAAAAG GAAGTTTGAGGGCCACTGGGAAAGAGAAGGGGTATCACCGCTTCCGGACCCCGGCCTGTACTT GAAGGCAAAGAGAACTACAAATCCCAGCGTCACCCGCGGCCTTGAAGCCCCGCCCCTGACAAA CTGAAGGTCCCGGTAAGCATCGCGTCAGTACTTATGGCGCCTGCCGGGTTGTGGTGACGAAAG CAGTTGCCATGGAGTTGCTCTGAGTAACCCTGAGGCAGTGGGACGCCAAGACTGGAGAGGAAG CGACTGCGGGTGAGTCGGGCGG SEQ ID NO: 8 An exemplary CMV promoter. TAGTTATTAATAGTAATCAATTACGGGGTCATTAGTTCATAGCCCATATATGGAGTTCCGCGTT ACATAACTTACGGTAAATGGCCCGCCTGGCTGACCGCCCAACGACCCCCGCCCATTGACGTCA ATAATGACGTATGTTCCCATAGTAACGCCAATAGGGACTTTCCATTGACGTCAATGGGTGGAGT ATTTACGGTAAACTGCCCACTTGGCAGTACATCAAGTGTATCATATGCCAAGTACGCCCCCTAT TGACGTCAATGACGGTAAATGGCCCGCCTGGCATTATGCCCAGTACATGACCTTATGGGACTTT CCTACTTGGCAGTACATCTACGTATTAGTCATCGCTATTACCATGGTGATGCGGTTTTGGCAGT ACATCAATGGGCGTGGATAGCGGTTTGACTCACGGGGATTTCCAAGTCTCCACCCCATTGACGT CAATGGGAGTTTGTTTTGGCACCAAAATCAACGGGACTTTCCAAAATGTCGTAACAACTCCGCC CCATTGACGCAAATGGGCGGTAGGCGTGTACGGTGGGAGGTCTATATAAGCAGAGCTGGTTTA GTGAACCGTCAGATC SEQ ID NO: 9 An exemplary CAG promoter. ACTAGTTATTAATAGTAATCAATTACGGGGTCATTAGTTCATAGCCCATATATGGAGTTCCGCG TTACATAACTTACGGTAAATGGCCCGCCTGGCTGACCGCCCAACGACCCCCGCCCATTGACGTC AATAATGACGTATGTTCCCATAGTAACGCCAATAGGGACTTTCCATTGACGTCAATGGGTGGAC TATTTACGGTAAACTGCCCACTTGGCAGTACATCAAGTGTATCATATGCCAAGTACGCCCCCTA TTGACGTCAATGACGGTAAATGGCCCGCCTGGCATTATGCCCAGTACATGACCTTATGGGACTT TCCTACTTGGCAGTACATCTACGTATTAGTCATCGCTATTACCATGGGTCGAGGTGAGCCCCAC GTTCTGCTTCACTCTCCCCATCTCCCCCCCCTCCCCACCCCCAATTTTGTATTTATTTATTTTTTA ATTATTTTGTGCAGCGATGGGGGCGGGGGGGGGGGGGGCGCGCGCCAGGCGGGGCGGGGCGG GGCGAGGGGCGGGGCGGGGCGAGGCGGAGAGGTGCGGCGGCAGCCAATCAGAGCGGCGCGCT CCGAAAGTTTCCTTTTATGGCGAGGCGGCGGCGGCGGCGGCCCTATAAAAAGCGAAGCGCGCG GCGGGCGGGAGTCGCTGCGTTGCCTTCGCCCCGTGCCCCGCTCCGCGCCGCCTCGCGCCGCCCG CCCCGGCTCTGACTGACCGCGTTACTCCCACAGGTGAGCGGGCGGGACGGCCCTTCTCCTCCGG GCTGTAATTAGCGCTTGGTTTAATGACGGCTCGTTTCTTTTCTGTGGCTGCGTGAAAGCCTTAAA GGGCTCCGGGAGGGCCCTTTGTGCGGGGGGGAGCGGCTCGGGGGGTGCGTGCGTGTGTGTGTG CGTGGGGAGCGCCGCGTGCGGCCCGCGCTGCCCGGCGGCTGTGAGCGCTGCGGGCGCGGCGCG GGGCTTTGTGCGCTCCGCGTGTGCGCGAGGGGAGCGCGGCCGGGGGCGGTGCCCCGCGGTGCG GGGGGGCTGCGAGGGGAACAAAGGCTGCGTGCGGGGTGTGTGCGTGGGGGGGTGAGCAGGGG GTGTGGGCGCGGCGGTCGGGCTGTAACCCCCCCCTGCACCCCCCTCCCCGAGTTGCTGAGCACG GCCCGGCTTCGGGTGCGGGGCTCCGTGCGGGGCGTGGCGCGGGGCTCGCCGTGCCGGGCGGGG GGTGGCGGCAGGTGGGGGTGCCGGGCGGGGCGGGGCCGCCTCGGGCCGGGGAGGGCTCGGGG8123-110315-03GAGGGGCGCGGCGGCCCCGGAGCGCCGGCGGCTGTCGAGGCGCGGCGAGCCGCAGCCATTGC CTTTTATGGTAATCGTGCGAGAGGGCGCAGGGACTTCCTTTGTCCCAAATCTGGCGGAGCCGAA ATCTGGGAGGCGCCGCCGCACCCCCTCTAGCGGGCGCGGGCGAAGCGGTGCGGCGCCGGCAG GAAGGAAATGGGCGGGGAGGGCCTTCGTGCGTCGCCGCGCCGCCGTCCCCTTCTCCATCTCCA GCCTCGGGGCTGCCGCAGGGGGACGGCTGCCTTCGGGGGGGACGGGGCAGGGCGGGGTTCGG CTTCTGGCGTGTGACCGGCGGCTCTAGAGCCTCTGCTAACCATGTTCATGCCTTCTTCTTTTTCC TACAGCTCCTGGGCAACGTGCTGGTTATTGTGCTGTCTCATCATTTTGGCAAA SEQ ID NO: 10 An exemplary Ef1α promoter. GGCTCCGGTGCCCGTCAGTGGGCAGAGCGCACATCGCCCACAGTCCCCGAGAAGTTGGGGGGA GGGGTCGGCAATTGAACCGGTGCCTAGAGAAGGTGGCGCGGGGTAAACTGGGAAAGTGATGT CGTGTACTGGCTCCGCCTTTTTCCCGAGGGTGGGGGAGAACCGTATATAAGTGCAGTAGTCGCC GTGAACGTTCTTTTTCGCAACGGGTTTGCCGCCAGAACACAGGTAAGTGCCGTGTGTGGTTCCC GCGGGCCTGGCCTCTTTACGGGTTATGGCCCTTGCGTGCCTTGAATTACTTCCACCTGGCTGCA GTACGTGATTCTTGATCCCGAGCTTCGGGTTGGAAGTGGGTGGGAGAGTTCGAGGCCTTGCGCT TAAGGAGCCCCTTCGCCTCGTGCTTGAGTTGAGGCCTGGCCTGGGCGCTGGGGCCGCCGCGTGC GAATCTGGTGGCACCTTCGCGCCTGTCTCGCTGCTTTCGATAAGTCTCTAGCCATTTAAAATTTT TGATGACCTGCTGCGACGCTTTTTTTCTGGCAAGATAGTCTTGTAAATGCGGGCCAAGATCTGC ACACTGGTATTTCGGTTTTTGGGGCCGCGGGCGGCGACGGGGCCCGTGCGTCCCAGCGCACAT GTTCGGCGAGGCGGGGCCTGCGAGCGCGGCCACCGAGAATCGGACGGGGGTAGTCTCAAGCT GGCCGGCCTGCTCTGGTGCCTGGTCTCGCGCCGCCGTGTATCGCCCCGCCCTGGGCGGCAAGGC TGGCCCGGTCGGCACCAGTTGCGTGAGCGGAAAGATGGCCGCTTCCCGGCCCTGCTGCAGGGA GCTCAAAATGGAGGACGCGGCGCTCGGGAGAGCGGGCGGGTGAGTCACCCACACAAAGGAAA AGGGCCTTTCCGTCCTCAGCCGTCGCTTCATGTGACTCCACGGAGTACCGGGCGCCGTCCAGGC ACCTCGATTAGTTCTCGAGCTTTTGGAGTACGTCGTCTTTAGGTTGGGGGGAGGGGTTTTATGC GATGGAGTTTCCCCACACTGAGTGGGTGGAGACTGAAGTTAGGCCAGCTTGGCACTTGATGTA ATTCTCCTTGGAATTTGCCCTTTTTGAGTTTGGATCTTGGTTCATTCTCAAGCCTCAGACAGTGG TTCAAAGTTTTTTTCTTCCATTTCAGGTGTCGTGA SEQ ID NO: 11 An exemplary Myo151 kb promoter. CTGCAGCTCAGCCTACTACTTGCTTTCCAGGCTGTTCCTAGTTCCCATGTCAGCTGCTTGTGCTT TCCAGAGACAAAACAGGAATAATAGATGTCATTAAATATACATTGGGCCCCAGGCGGTCAATG TGGCAGCCTGAGCCTCCTTTCCATCTCTGTGGAGGCAGACATAGGACCCCCAACAAACAGCAT GCAGGTTGGGAGCCAGCCACAGGACCCAGGTAAGGGGCCCTGGGTCCTTAAGCTTCTGCCACT GGCTCCGGCATTGCAGAGAGAAGAGAAGGGGCGGCAGACTGGAGAGCTGGGCTCCATTTTTGT TCCTTGGTGCCCTGCCCCTCCCCATGACCTGCAGAGACATTCAGCCTGCCAGGCTTTATGAGGT GGGAGCTGGGCTCTCCCTGATGTATTATTCAGCTCCCTGGAGTTGGCCAGCTCCTGTTACACTG GCCACAGCCCTGGGCATCCGCTTCTCACTTCTAGTTTCCCCTCCAAGGTAATGTGGTGGGTCAT GATCATTCTATCCTGGCTTCAGGGACCTGACTCCACTTTGGGGCCATTCGAGGGGTCTAGGGTA GATGATGTCCCCCTGTGGGGATTAATGTCCTGCTCTGTAAAACTGAGCTAGCTGAGATCCAGGA GGGCTTGGCCAGAGACAGCAAGTTGTTGCCATGGTGACTTTAAAGCCAGGTTGCTGCCCCAGC ACAGGCCTCCCAGTCTACCCTCACTAGAAAACAACACCCAGGCACTTTCCACCACCTCTCAAAG GTGAAACCCAAGGCTGGTCTAGAGAATGAATTATGGATCCTCGCTGTCCGTGCCACCCAGCTA GTCCCAGCGGCTCAGACACTGAGGAGAGACTGTAGGTTCAGCTACAAGCAAAAAGACCTAGCT GGTCTCCAAGCAGTGTCTCCAAGTCCCTGAACCTGTGACACCTGCCCCAGGCATCATCAGGCAC AGAGGGCCACC SEQ ID NO: 12 An exemplary nucleic acid sequence encoding mouse TOMT protein. ATGTCCCCTGCCATTGCACTGGCATTCCTGCCACTCGTGGTAACACTGCTGGTGAGATACCGGC ACCATTTCCGACTGCTGGTGCGTACAGTCCTGCTGAGAGGATTTCGAGACTGCCTGTCAGGACT TCGGATTGAGGAGCGGGCTTTCAGCTATGTGCTCACCCATGCCCTGCCTGGAGACCCTGGTCAC ATCCTCACCACGCTTGACCATTGGAGCAGCTGCTGCGAGTACCTGAGCCACATGGGCCCTGTTA AAGGTCAGATTCTGATGCGGCTGGTGGAAGAGAAGGCCCCTGCTTGTGTGCTGGAGCTGGGCA8123-110315-03CATACTGTGGATACTCTACACTGCTTATTGCGCGAGCCTTGCCCCCTGGAAGTCGCCTTCTCACT GTGGAGCGGGACTCACGTACAGCAGCAGTGGCTGAAAAAGTCATCCGGCTGGCAGGCTTCGAT GAGCAAATGGTGGAGCTCATTGCAGGCAGCTCAGAGGAAGTGATCCCACGCCTAAGAGCTCAG CACCAGCTGAATCGTGCAGATCTGGTGCTCCTGGCACACCGACCTCGGTATTACTTAAGGGATC TGCAGCTACTGGAGGCCCATGCTCTGCTCCCACATGGCGCCACTGTATTGGCTGACCATGTGCT TTTTCCTGGTGCACCCCGCTTCCTACAGTACACCAAGAGCTGTGGTCGCTATCGCTGCCGCCTTC ACCACACCAGCCTCCCAGACTTCCCTGCCATTAAAGATGGCATAGCCCAACTCACCTATACTGG ACCCGGCTGA SEQ ID NO: 13 An exemplary human TOMT amino acid sequence. MGTPWRKRKGIAGPGLPDLSCALVLQPRAQVGTMSPAIALAFLPLVVTLLVRYRHYFRLLVRTVLL RSLRDCLSGLRIEERAFSYVLTHALPGDPGHILTTLDHWSSRCEYLSHMGPVKGQILMRLVEEKAPA CVLELGTYCGYSTLLIARALPPGGRLLTVERDPRTAAVAEKLIRLAGFDEHMVELIVGSSEDVIPCLR TQYQLSRADLVLLAHRPRCYLRDLQLLEAHALLPAGATVLADHVLFPGAPRFLQYAKSCGRYRCR LHHTGLPDFPAIKDGIAQLTYAGPG* SEQ ID NO: 14 An exemplary nucleic acid sequence encoding human TOMT protein. ATGGGAACCCCATGGAGGAAGAGAAAGGGTATAGCAGGCCCTGGACTCCCCGACCTGTCCTGT GCTCTGGTCCTCCAGCCCAGGGCCCAGGTAGGGACCATGTCCCCTGCCATTGCATTGGCCTTCC TGCCACTGGTGGTAACATTGCTGGTGCGGTACCGGCACTACTTCCGATTGCTGGTGCGCACGGT CTTGCTGCGAAGCCTCCGAGACTGCCTGTCAGGGCTGCGGATCGAGGAGCGGGCCTTCAGCTA CGTGCTCACCCATGCCCTGCCCGGTGACCCTGGTCACATCCTCACCACCCTGGACCACTGGAGC AGCCGCTGCGAGTACTTGAGCCACATGGGGCCTGTCAAAGGTCAGATCCTGATGCGGCTGGTG GAGGAGAAGGCCCCTGCTTGTGTGCTGGAATTGGGAACCTACTGTGGATACTCTACCCTGCTTA TTGCCCGAGCCCTGCCCCCTGGGGGTCGCCTTCTTACTGTGGAGCGGGACCCACGCACGGCAGC AGTGGCTGAAAAACTCATCCGCCTGGCCGGCTTTGATGAGCACATGGTGGAGCTCATCGTGGG CAGCTCAGAGGACGTGATCCCGTGCCTACGCACCCAGTATCAGCTGAGTCGGGCAGACCTGGT GCTCCTGGCACACCGGCCACGATGTTACCTGAGGGACCTGCAGCTGCTGGAGGCCCATGCCCT ACTGCCAGCAGGTGCCACCGTGCTGGCTGACCATGTGCTCTTCCCTGGTGCACCCCGCTTCTTG CAGTATGCTAAGAGCTGTGGCCGCTACCGCTGCCGCCTCCACCACACTGGCCTTCCAGACTTCC CTGCCATCAAGGATGGAATAGCTCAGCTCACCTATGCTGGACCAGGCTGA SEQ ID NO: 15 An exemplary mouse TOMT amino acid sequence. MSPAIALAFLPLVVTLLVRYRHHFRLLVRTVLLRGFRDCLSGLRIEERAFSYVLTHALPGDPGHILTT LDHWSSCCEYLSHMGPVKGQILMRLVEEKAPACVLELGTYCGYSTLLIARALPPGSRLLTVERDSR TAAVAEKVIRLAGFDEQMVELIAGSSEEVIPRLRAQHQLNRADLVLLAHRPRYYLRDLQLLEAHAL LPHGATVLADHVLFPGAPRFLQYTKSCGRYRCRLHHTSLPDFPAIKDGIAQLTYTGPG* DETAILED DESCRIPTION Although many methods and materials similar or equivalent to those described herein can be used, particular suitable methods and materials are described herein. The materials, methods, and examples provided are illustrative only and not intended to be limiting. In case of conflict, the present specification, including explanations of terms, will control. I. Introduction Hearing loss is one of the most common sensory deficits.1 in 1000 children are born with hereditary hearing loss (genetic hearing loss), often affecting hair cells within the cochlea of the inner ear. A disruption of the structure and / or function of the inner ear can also cause vestibular disorders. Thus, people who have8123-110315-03hereditary hearing loss also commonly experience vestibular disorders. Mutations in Transmembrane-O- methyltransferase (TOMT, also known as COMT2 or LRTOMT) cause profound deafness in humans, mice, and zebrafish. The Tomt gene regulatory landscape (promoters, enhancers, etc.) is unknown, however, Tomt mRNA and protein are expressed specifically in cochlear and vestibular hair cells. As shown herein, Tomt mutant mice also show symptoms of vestibular disorder. Here, unique Tomt regulatory elements that specifically express in cochlear hair cells were identified. These fragments were used to generate a novel adeno-associated viral (AAV) vector containing a Tomt promoter fragment operably linked to a gene of interest (e.g., wild-type TOMT gene). With this novel vector, efficient, comprehensive, and selective expression in cochlear hair cells was achieved without cellular toxicity or expression in off-target cell types. When utilized for gene therapy, substantial hearing rescue was achieved in profoundly deaf mice. Gene therapy was also found to rescue vestibular function of these mice. The results disclosed herein are much improved over existing vectors, particularly those using ubiquitous promoters. The unique Tomt promoter fragments and vectors described herein are compatible for gene therapy using any gene that, when specifically expressed in cochlear hair cells, could treat hereditary hearing loss and / or vestibular disorders. II. Summary of Terms Unless otherwise noted, technical terms are used according to conventional usage. Definitions of many common molecular biology terms may be found in Krebs et al. (eds.), Lewin’s genes XII, published by Jones & Bartlett Learning, 2017. As used herein, the singular forms “a,” “an,” and “the,” refer to both the singular as well as plural, unless the context clearly indicates otherwise. For example, the term “a nucleic acid” includes singular or plural nucleic acids and can be considered equivalent to the phrase “at least one nucleic acid.” As used herein, the term “comprises” means “includes.” It is further to be understood that any and all base sizes or amino acid sizes, and all molecular weight or molecular mass values, given for nucleic acids or polypeptides are approximate, and are provided for descriptive purposes, unless otherwise indicated. To facilitate review of the disclosure, the following explanations of terms are provided: About: Unless context indicates otherwise, “about” refers to plus or minus 5% of a reference value. For example, “about” 100 refers to the range of 95 to 105. Adeno-associated virus (AAV): A replication-defective, non-enveloped virus that infects humans and some other primate species. AAV is not known to cause disease and elicits a very mild immune response. Gene therapy vectors that utilize AAV can infect both dividing and quiescent cells and can persist in an extrachromosomal state without integrating into the genome of the host cell. These features make AAV a suitable vector for gene therapy. There are several recognized serotypes of AAV (e.g., AAV1, AAV2, AAV3, AAV4, AAV5, AAV6, AAV7, AAV8, AAV9, AAV10, AAV11, AAV12, AAV13, AAV- DJ, PhP.eB, 2.7m8, DJ / 8, rh10, and AAV-PHP.S). Administration: The introduction of an agent, such as a nucleic acid or vector for gene therapy, by an effective route. Exemplary routes of administration include, but are not limited to, oral, injection (such as8123-110315-03subcutaneous, intramuscular, intradermal, intraperitoneal, intravenous, and intratympanic), sublingual, transdermal, intranasal, and inhalation routes. Administration can be local or systemic. Local administration refers to the introduction of an agent directly to a desired a site of action, for example, administering a gene therapy vector to a particular bodily location, for example, local delivery to the inner ear (e.g., through the posterior semicircular canal or round window). Systemic administration refers to the introduction of an agent into the circulatory system. Agent: A substance, such as a nucleic acid, vector, protein, or other molecule of interest. A therapeutic agent is a substance that demonstrates a therapeutic effect by restoring or maintaining health, such as by alleviating symptoms associated with a disease or condition, or by delaying (inhibiting) progression or onset of a disease or condition (e.g., hearing loss and / or vestibular disorders). A therapeutic agent can include a recombinant nucleic acid or vector disclosed herein. Cochlear Hair Cell: A specialized cell located in the cochlea and vestibule, which functions as a sensory receptor of both the auditory and vestibular systems. Mammalian cochlear hair cells include two distinct types, outer hair cells (OHCs) and inner hair cells (IHCs), while mammalian vestibular hair cells include Type I and Type II hair cells. Damage to hair cells can result in decreased hearing sensitivity and / or difficulties with balance (via perturbations to the vestibular system). Outer hair cells in the cochlea mechanically amplify low-level sound that enters the cochlea to nonlinearly amplify quiet sounds. This mechanism allows a wide range of sound pressures to be reduced to a smaller range of hair displacements. The inner hair cells transform sound vibrations in the fluids of the cochlea into electrical signals that are relayed via the auditory nerve to the auditory brainstem and to the auditory cortex. Contacting: Placing an agent in direct physical association, including both in solid and liquid form, and can take place either in vivo or in vitro. Contacting includes contacting a cell (e.g., a cochlear hair cell) by placing an agent (e.g., a nucleic acid or vector disclosed here) in direct physical association with the cell. Control: A reference standard. A control can be a positive or negative control. In some examples, the control is a measurement (e.g., measurement of hearing and / or vestibular function in a subject, or expression of a gene associated with hearing loss and / or vestibular disorders) obtained prior to administering an agent to a subject or cell (e.g., introducing a recombinant nucleic acid and / or vector disclosed herein). In some examples, the control is a historical control or a standard reference or range (e.g., a typical measurement or range observed for a particular population, such as a measurement of hearing and / or vestibular function, or expression of a gene associated with hearing loss in a deaf population or a non-deaf population). Degenerate Variant: A nucleic acid sequence variant due to degeneracy (redundancy) of the genetic code. While the nucleic acid sequence of a degenerate variant differs from a reference sequence, the degenerate variant and reference sequence encode the same amino acid sequence. Expression (of a nucleic acid): Producing a product (e.g., protein or RNA) encoded by the nucleic acid.8123-110315-03Exogenous: Originating from outside a reference organism source. For example, a nucleic acid molecule that is exogenous to a cell is a nucleic acid that originated from a source other than the cell itself (e.g., an artificial nucleic acid, such as a recombinant nucleic acid). Heterologous: A nucleic acid or protein derived from a different origin or source as a reference. For example, an artificial TOMT gene (e.g., CDS or cDNA sequence) is heterologous to a TOMT regulatory element because these sequences do not naturally occur together on the same nucleic acid molecule. Host Cell: Cells that are transformed, or capable of being transformed, by an exogenous / heterologous nucleic acid or vector. The cells can be prokaryotic or eukaryotic. The term also includes progeny cells that include the exogenous / heterologous nucleic acid or vector. Increase or Decrease: A positive (increase) or negative (decrease) difference relative to a reference value, such as a control. A difference can be a qualitative or quantitative. In some examples, the difference is statistically significant (e.g., P-value less than 0.05 or 0.01). In some examples, the difference is an increase relative to a control of at least 5%, such as at least 10%, at least 20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 100%, at least 150%, at least 200%, at least 250%, at least 300%, at least 350%, at least 400%, at least 500%, or greater than 500%. In some examples, the difference is a decrease relative to a control of at least 5%, such as at least 10%, at least 20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95%, at least 98%, or 100%. Isolated or Purified: An “isolated” or “purified” biological component (such as a nucleic acid or protein) is one that has been substantially separated from other biological components in the environment in which the component occurs, e.g., separated from other chromosomal and extra-chromosomal DNA and RNA, proteins and / or cells. Nucleic acids and proteins that have been “isolated” include nucleic acids and proteins purified by standard purification methods. The term embraces nucleic acids and proteins prepared by recombinant expression in a host cell as well as chemically synthesized nucleic acids. Absolute purity or isolation is not required, it is intended as a relative term. Thus, for example, a purified / isolated protein, nucleic acid, or cell preparation is one in which the protein, nucleic acid, or cell is more enriched than the protein, nucleic acid, or cell is in its initial environment. In one example, a preparation is purified / isolated such that the protein, nucleic acid, or cell represents at least 50% of the total content of the preparation. In some examples, an isolated nucleic acid (or vector) is at least 60%, at least 70%, at least 80%, at least 90%, at least 95%, at least 98%, or at least 99% pure. In a specific, non-limiting example, an isolated nucleic acid (or vector) is 90% free of other components. Operably Linked: A nucleic acid sequence is “operably linked” when it is placed in a functional relationship with a second nucleic acid sequence. For instance, a promoter (or promoter fragment) is operably linked to a coding sequence if the promoter (or promoter fragment) affects the transcription or expression of the coding sequence. Generally, operably linked DNA sequences are contiguous and, where necessary to join two protein-coding regions, are in the same reading frame.8123-110315-03Pharmaceutically Acceptable Carriers: The pharmaceutically acceptable carriers of use for the compositions and methods disclosed herein are known. In general, the nature of a carrier depends on the particular mode of administration being employed. For instance, injection formulations may include injectable fluids that include pharmaceutically and physiologically acceptable fluids such as water, physiological saline, balanced salt solutions, aqueous dextrose, glycerol, or the like as a vehicle. Transdermal formulations may include petroleum jelly, petroleum wax, glycerol, hydrophobic surfactants, etc. Suitable carriers are described, for example, in Remington’s Pharmaceutical Sciences, 23rd Edition, Academic Press, Elsevier, (2020). Promoter: A nucleic acid control sequence that directs transcription of an operably linked nucleic acid. A promoter includes necessary nucleic acid sequences near the start site of transcription. A promoter also optionally includes distal enhancer or repressor elements. A “constitutive promoter” is a promoter that is continuously active and is not subject to regulation by external signals or molecules. In contrast, the activity of an “inducible promoter” is regulated by an external signal or molecule. Promoters also include cell or tissue specific promoters, which are only active in particular cell or tissue types. In some examples, the nucleic acids and / or vectors provided herein include a Tomt promoter or a Tomt promoter fragment. Promoter fragment, as used herein, includes sequences derived from a known or predicted promoter sequence that retains promoter function (transcriptional activity). Recombinant: A nucleic acid or protein that has a sequence made by an artificial combination of two otherwise separated segments of sequence (e.g., a “chimeric” sequence). This artificial combination can be accomplished by chemical synthesis or by manipulation of isolated segments of nucleic acids, for example, by standard molecular biology techniques (e.g., cloning). Regulatory Element: A term that includes promoters, enhancers, internal ribosomal entry sites (IRES), and other expression control elements. Regulatory elements include those that direct constitutive expression of a nucleotide sequence in many types of host cells and those that direct expression of the nucleotide sequence only in certain host cells (e.g., tissue-specific regulatory sequences). Regulatory elements may also direct expression in a temporal-dependent manner, such as in a cell-cycle dependent or developmental stage-dependent manner, which may or may not also be tissue or cell-type specific. Sequence Identity: The degree of similarity between amino acid or nucleic acid sequences. Sequence identity is frequently measured in terms of percentage identity (or percent identity); the higher the percentage, the more similar the two sequences are. Homologs of a polypeptide (or nucleotide sequence) will possess a relatively high degree of sequence identity when aligned using standard methods. Methods of alignment of sequences for comparison have been described. The NCBI Basic Local Alignment Search Tool (BLAST®) tool is often used and is available from several sources, including the National Center for Biotechnology Information (blast.ncbi.nlm.nih.gov / Blast.cgi). Various types of BLAST® are available, for example, blastp, blastn, blastx, tblastn, tblastx, and psiblast. A description of how to determine sequence identity using this program is available on the NCBI website and other resources. In some8123-110315-03examples, percent sequence identity is determined using default query parameters, for example, parameters provided below is Table 1. Table 1: Exemplary default parameters for BLAST programs. BLASTN BLASTP BLASTX TBLASTN TBLASTX PSIBLAST Gap Opening Plt5 11 11 11 11 5 rodents, pigs, sheep, cows, and the like which is to be the recipient of a treatment provided herein. In some examples, the subject is a veterinary subject (e.g., non-human primate, domestic cat, domestic dog, mouse, or rat). In a non-limiting example, the subject is a human subject, such as one with hearing loss, for example, hearing loss due to a genetic mutation, and / or vestibular disorder. Therapeutically Effective Amount: The amount of a therapeutic agent (e.g., a nucleic acid and / or vector for gene therapy) sufficient to achieve a desired effect in a subject, or in a cell, being treated with the agent, such as improving hearing and / or vestibular function. The exact amount and timing of administration can depend on a number of factors, including the subject being treated, the severity and type of the condition being treated, and the manner of administration. A therapeutically effective amount can be determined by a practitioner, for example, through clinical trials or various in vitro, in vivo or in situ assays. Transformed: A transformed cell is a cell into which an exogenous nucleic acid molecule has been introduced by a molecular biology technique. As used herein, the term transformation encompasses all techniques by which a nucleic acid molecule might be introduced into a cell, including chemical methods (e.g., calcium-phosphate transfection), physical methods (e.g., electroporation, microinjection, particle bombardment), fusion (e.g., liposomes), lipofection, nucleofection, receptor-mediated endocytosis (e.g., DNA-protein complexes, viral envelope / capsid-DNA complexes), biolistics (particle gun accelerator or gene gun), or other transduction and / or transfection methods. Transgene: An exogenous gene supplied by a vector. Transmembrane O-Methyltransferase (TOMT): The TOMT gene encodes a catechol-O- methyltransferase that is important for auditory and vestibular function. Mutations in TOMT have been associated with nonsyndromic deafness. TOMT is specifically expressed in cochlear hair cells. Sequence information for TOMT is known, see, e.g., NCBI Gene ID 120356740 (ncbi.nlm.nih.gov / gene / 120356740). TOMT is also sometimes referred to as LRTOMT or COMT. The TOMT promoter has not yet been defined. Treating or Inhibiting (a disease or condition): Treatment refers to a therapeutic intervention that ameliorates a sign or symptom of a disease or condition (e.g., hearing loss or vestibular disorder) after the disease or condition has begun to develop. The term “ameliorating,” with reference to a disease or8123-110315-03condition, refers to any observable beneficial effect of the treatment. The beneficial effect can be evidenced, for example, by a delayed onset of symptoms in a subject, a reduction in severity of some or all symptoms (e.g., hearing loss or vestibular disorder), a slower progression, an improvement in the quality of life of the subject, or by other parameters that are specific to the particular disease or condition. Treatment may be assessed by objective or subjective parameters, including the results of a physical examination, hearing tests, imaging, or other clinical tests, as well as self-evaluations by the subject. Inhibiting a disease or condition includes reducing the risk of the disease or condition, such as reducing the risk of hearing loss and / or vestibular disorder. A “prophylactic” treatment is a treatment administered to a subject who does not exhibit signs of a disease, or exhibits only early signs, for the purpose of decreasing the risk of further developing a disease or condition. In some examples, the disclosed methods are prophylactic and / or therapeutic. In some examples, the disclosed methods are therapeutic and not prophylactic. Vector: A nucleic acid molecule as introduced into a host cell, thereby producing a transformed host cell. A vector may include nucleic acid sequences that permit it to replicate in the host cell, such as an origin of replication, or one or more regulatory elements. A vector may also include one or more therapeutic genes and / or selectable marker genes and other genetic elements known in the art. A vector can be used to transduce, transform or infect a cell, thereby causing the cell to express non-native nucleic acids. A vector optionally includes materials to aid in achieving entry of the nucleic acid into the cell, such as a viral particle, liposome, protein coating, or the like. In some examples herein, the vector is an AAV vector. Vestibular Disorder: A condition that typically affects balance and / or sense of orientation due to a disruption in the vestibular system. The vestibular system is a complex set of structures and neural pathways that together contribute to the sense of proprioception and equilibrium. The vestibular system includes sensory organs in the inner ear that monitor the motion and position of the head in space. Symptoms of vestibular disorders include vertigo, nausea, vomiting, intolerance to head motion, unsteady gait, difficulty walking (e.g., circling), postural instability, and nystagmus. III. Compositions Disclosed are recombinant nucleic acid molecules comprising a transmembrane-O- methyltransferase (TOMT) regulatory element operably linked to a nucleic acid molecule. In some examples, the TOMT regulatory element is a mammalian TOMT regulatory element, for example, a mouse Tomt regulatory element or a human TOMT regulatory element. In some examples, the regulatory element is a TOMT promoter and / or enhancer. In some examples, the TOMT regulatory element includes one or more enhancers, such as 1, 2, 3, 4, or 5 enhancer elements. In some examples, the TOMT regulatory element is a fragment of a native TOMT promoter (e.g., a wild-type sequence), for example, a TOMT promoter fragment as shown in SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7. The native human TOMT promoter may be located between positions 72,078,681-72,111,197 on chromosome 11. The native mouse Tomt promoter may be located between positions 101,898,299-8123-110315-03101,906,487 on chromosome 7, for example, between positions 101,898,200-101,907,299 on chromosome 7. In some examples, the TOMT regulatory element is a 50 to 2700 nucleotide (nt) fragment of a native TOMT promoter, for example, about 50 to about 2000, about 50 to about 1500, about 50 to about 1250, about 50 to about 1200, about 50 to about 1120, about 50 to about 1100, about 50 to about 1000, about 50 to about 900, about 50 to about 800, about 50 to about 700, about 50 to about 600, about 50 to about 500, about 50 to about 400, about 50 to about 300, or about 50 to about 200, about 75 to about 2000, about 75 to about 1500, about 75 to about 1250, about 75 to about 1200, about 75 to about 1120, about 75 to about 1100, about 75 to about 1000, about 75 to about 900, about 75 to about 800, about 75 to about 700, about 75 to about 600, about 75 to about 500, about 75 to about 400, about 75 to about 300, or about 75 to about 200 nucleotides. In some examples, the TOMT regulatory element is a sequence fragment of at least 50 contiguous nucleotides (e.g., at least 75 contiguous nucleotides, at least 526 contiguous nucleotides, etc.) located between positions 72,079,861-72,080,898 on human chromosome 11 (e.g., SEQ ID NO: 7). The TOMT regulatory elements can include one or more mutations relative to a native sequence, such as nucleotide deletions, substitutions, additions, or combinations thereof, so long as native function (e.g., promoter activity) is retained. In some examples, up to 5% (for example, up to 4%, up to 3%, up to 2%, or up to 1%) of the sequence of the TOMT regulatory element includes deletions, substitutions, or additions relative to a native sequence. In some examples, the sequence of the TOMT regulatory element is optimized for expression in cochlear and / or vestibular hair cells. In several implementations, the TOMT regulatory element induces expression of an operably linked nucleic acid molecule in hair cells (including cochlear and / or vestibular hair cells). In several implementations, the TOMT regulatory element induces expression of an operably linked nucleic acid molecule in cochlear and / or vestibular hair cells. In several implementations, the TOMT regulatory element induces expression of an operably linked nucleic acid molecule specifically in cochlear hair cells (e.g., does not significantly express the operably linked nucleic acid molecule in cells other than cochlear or vestibular hair cells). In some implementations, the TOMT regulatory element does not induce expression of an operably linked nucleic acid in neuronal cells. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides, such as at least 75, at least 100, at least 150, at least 200, at least 250, at least 300, at least 350, at least 400, at least 450, at least 500, at least 600, at least 700, at least 800, at least 900, at least 1000 or more contiguous nucleotides of SEQ ID NO: 1. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides, such as at least 75, at least 100, at least 150, at least 200, at least 250, at least 300, at least 350, at least 400, at least 450, at least 500, at least 600, at least 700, at least 800, at least 900, at least 1000, at least 1100, at least 1200, at least 1300, at least 1400, at least 1500, at least 1600, at least 1700, at least 1800, at least 1900, at least 2000, at least 2100, at least 2200, at least 2300, or more contiguous nucleotides of SEQ ID NO: 2. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides, such as at least 75, at least 100, at least 150, at least 200, at least 250, at least 300, at least 350, at least 400, at least 450, at least 500, at least 600, at least 700, or more contiguous nucleotides of SEQ ID NO: 3. In some examples, the TOMT regulatory element includes at least 50 contiguous8123-110315-03nucleotides, such as at least 75, at least 100, at least 150, at least 200, at least 250, at least 300, at least 350, at least 400, at least 450, at least 500, at least 600, at least 700, at least 800, at least 900, at least 1000, at least 1100, at least 1200, or more contiguous nucleotides of SEQ ID NO: 4. In some examples, the TOMT regulatory element includes at least 25 contiguous nucleotides, such as at least 30, at least 40, at least 50, at least 60, at least 70, or more contiguous nucleotides of SEQ ID NO: 5. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides, such as at least 75, at least 100, at least 150, at least 200, at least 250, at least 300, at least 350, at least 400, at least 450, at least 500, or more contiguous nucleotides of SEQ ID NO: 6. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides, such as at least 75, at least 100, at least 150, at least 200, at least 250, at least 300, at least 350, at least 400, at least 450, at least 500, at least 600, at least 700, at least 800, at least 900, at least 950 or more contiguous nucleotides of SEQ ID NO: 7. The TOMT regulatory element is a size suitable for use in known gene therapy vectors. In some examples, the TOMT regulatory element includes no more than 3500 nucleotides, for example, no more than 3000, no more than 2500, no more than 2000, no more than 1750, no more than 1500, no more than 1250, no more than 1125, no more than 1050, no more than 1000, no more than 750, no more than 550, no more than 500, no more than 250, or no more than 100 nucleotides. In some examples, the TOMT regulatory element includes about 50 to about 2700 nucleotides, for example, 50 to 2500, 50 to 2250, 50 to 2000, 50 to 1750, 50 to 1500, 50 to 1250, 50 to 1125, 50 to 1050, 50 to 1000, 50 to 750, 50 to 550, 50 to 500, 50 to 250, 50 to 200, 50 to 150, 50 to 100, 50 to 75, 75 to 2500, 75 to 2250, 75 to 2000, 75 to 1750, 75 to 1500, 75 to 1250, 75 to 1125, 75 to 1050, 75 to 1000, 75 to 750, 75 to 550, 75 to 500, 75 to 300, 75 to 250, 75 to 200, 75 to 150, or 75 to 100 nucleotides. In some examples, the TOMT regulatory element includes at least 50 consecutive nucleotides of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7. In some examples, the TOMT regulatory element includes at least 75 consecutive nucleotides of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7. In some examples, the TOMT regulatory element includes at least 500 consecutive nucleotides of SEQ ID NO: 1, 2, 3, 4, 6, or 7. In some examples, the TOMT regulatory element includes at least 700 consecutive nucleotides of SEQ ID NO: 1, 2, 3, 4, or 7. In some examples, the TOMT regulatory element includes at least 1000 consecutive nucleotides of SEQ ID NO: 1, 2, 4, or 7. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides of SEQ ID NO: 1. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides of SEQ ID NO: 2. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides of SEQ ID NO: 3. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides of SEQ ID NO: 4. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides of SEQ ID NO: 5. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides of SEQ ID NO: 6. In some examples, the TOMT regulatory element includes at least 50 contiguous nucleotides of SEQ ID NO: 7. In some examples, the TOMT regulatory element includes at least 75 contiguous nucleotides of SEQ ID NO: 1. In some examples, the TOMT regulatory8123-110315-03element includes at least 75 contiguous nucleotides of SEQ ID NO: 2. In some examples, the TOMT regulatory element includes at least 75 contiguous nucleotides of SEQ ID NO: 3. In some examples, the TOMT regulatory element includes at least 75 contiguous nucleotides of SEQ ID NO: 4. In some examples, the TOMT regulatory element includes at least 75 contiguous nucleotides of SEQ ID NO: 5. In some examples, the TOMT regulatory element includes at least 75 contiguous nucleotides of SEQ ID NO: 6. In some examples, the TOMT regulatory element includes at least 75 contiguous nucleotides of SEQ ID NO: 7. In some examples, the TOMT regulatory element includes at least 100 contiguous nucleotides of SEQ ID NO: 1. In some examples, the TOMT regulatory element includes at least 100 contiguous nucleotides of SEQ ID NO: 2. In some examples, the TOMT regulatory element includes at least 100 contiguous nucleotides of SEQ ID NO: 3. In some examples, the TOMT regulatory element includes at least 100 contiguous nucleotides of SEQ ID NO: 4. In some examples, the TOMT regulatory element includes at least 100 contiguous nucleotides of SEQ ID NO: 6. In some examples, the TOMT regulatory element includes at least 100 contiguous nucleotides of SEQ ID NO: 7. In some examples, the TOMT regulatory element includes as least 500 contiguous nucleotides of SEQ ID NO: 1. In some examples, the TOMT regulatory element includes as least 500 contiguous nucleotides of SEQ ID NO: 2. In some examples, the TOMT regulatory element includes as least 500 contiguous nucleotides of SEQ ID NO: 3. In some examples, the TOMT regulatory element includes as least 500 contiguous nucleotides of SEQ ID NO: 4. In some examples, the TOMT regulatory element includes as least 500 contiguous nucleotides of SEQ ID NO: 6. In some examples, the TOMT regulatory element includes as least 500 contiguous nucleotides of SEQ ID NO: 7. In some examples, the TOMT regulatory element includes as least 1000 contiguous nucleotides of SEQ ID NO: 1. In some examples, the TOMT regulatory element includes as least 1000 contiguous nucleotides of SEQ ID NO: 2. In some examples, the TOMT regulatory element includes as least 1000 contiguous nucleotides of SEQ ID NO: 4. In some examples, the TOMT regulatory element includes as least 1000 contiguous nucleotides of SEQ ID NO: 7. In some examples, the TOMT regulatory element includes about 50 to about 1100 contiguous nucleotides of SEQ ID NO: 1, for example, 50 to 1000, 50 to 950, 50 to 900, 50 to 850, 50 to 800, 50 to 750, 50 to 700, 50 to 650, 50 to 600, 50 to 550, 50 to 500, 50 to 450, 50 to 400, 50 to 350, 50 to 300, 50 to 250, 50 to 200, 50 to 150, 50 to 100, 75 to 1100, 75 to 1000, 75 to 950, 75 to 900, 75 to 850, 75 to 800, 75 to 750, 75 to 700, 75 to 650, 75 to 600, 75 to 550, 75 to 500, 75 to 450, 75 to 400, 75 to 350, 75 to 300, 75 to 250, 75 to 200, 75 to 150, 75 to 100, 100 to 1100, 100 to 1000, 100 to 950, 100 to 900, 100 to 850, 100 to 800, 100 to 750, 100 to 700, 100 to 650, 100 to 600, 100 to 550, 100 to 500, 100 to 450, 100 to 400, 100 to 350, 100 to 300, 100 to 250, 100 to 200, 100 to 150, 200 to 1100, 200 to 1000, 200 to 950, 200 to 900, 200 to 850, 200 to 800, 200 to 750, 200 to 700, 200 to 650, 200 to 600, 200 to 550, 200 to 500, 200 to 450, 200 to 400, 200 to 350, 200 to 300, 200 to 250, 300 to 1100, 300 to 1000, 300 to 950, 300 to 900, 300 to 850, 300 to 800, 300 to 750, 300 to 700, 300 to 650, 300 to 600, 300 to 550, 300 to 500, 300 to 450, 300 to 400, 300 to 350, 400 to 1100, 400 to 1000, 400 to 950, 400 to 900, 400 to 850, 400 to 800, 400 to 750, 400 to 700, 400 to 650, 400 to 600, 400 to 550, 400 to 500, 400 to 450, 500 to 1100, 500 to 1000, 500 to 950, 500 to8123-110315-03900, 500 to 850, 500 to 800, 500 to 750, 500 to 700, 500 to 650, 500 to 600, 500 to 550, 600 to 1100, 600 to 1000, 600 to 950, 600 to 900, 600 to 850, 600 to 800, 600 to 750, 600 to 700, 600 to 650, 700 to 1100, 700 to 1000, 700 to 950, 700 to 900, 700 to 850, 700 to 800, 700 to 750, 800 to 1100, 800 to 1000, 800 to 950, 800 to 900, 800 to 850, 900 to 1100, 900 to 1000, 900 to 950, 950 to 1100, or 950 to 1000 contiguous nucleotides of SEQ ID NO: 1. In some examples, the TOMT regulatory element includes about 50 to about 2400 contiguous nucleotides of SEQ ID NO: 2, for example, 50 to 2300, 50 to 2200, 50 to 2100, 50 to 2000, 50 to 1900, 50 to 1800, 50 to 1700, 50 to 1600, 50 to 1500, 50 to 1400, 50 to 1300, 50 to 1200, 50 to 1100, 50 to 1000, 50 to 900, 50 to 800, 50 to 700, 50 to 600, 50 to 500, 50 to 400, 50 to 300, 50 to 200, 50 to 100, 250 to 2300, 250 to 2200, 250 to 2100, 250 to 2000, 250 to 1900, 250 to 1800, 250 to 1700, 250 to 1600, 250 to 1500, 250 to 1400, 250 to 1300, 250 to 1200, 250 to 1100, 250 to 1000, 250 to 900, 250 to 800, 250 to 700, 250 to 600, 250 to 500, 250 to 400, 250 to 300, 500 to 2300, 500 to 2200, 500 to 2100, 500 to 2000, 500 to 1900, 500 to 1800, 500 to 1700, 500 to 1600, 500 to 1500, 500 to 1400, 500 to 1300, 500 to 1200, 500 to 1100, 500 to 1000, 500 to 900, 500 to 800, 500 to 700, 500 to 600, 1000 to 2300, 1000 to 2200, 1000 to 2100, 1000 to 2000, 1000 to 1900, 1000 to 1800, 1000 to 1700, 1000 to 1600, 1000 to 1500, 1000 to 1400, 1000 to 1300, 1000 to 1200, 1000 to 1100, 1500 to 2300, 1500 to 2200, 1500 to 2100, 1500 to 2000, 1500 to 1900, 1500 to 1800, 1500 to 1700, 1500 to 1600, 2000 to 2300, 2000 to 2200, or 2000 to 2100 contiguous nucleotides of SEQ ID NO: 2. In some examples, the TOMT regulatory element includes about 50 to about 700 contiguous nucleotides of SEQ ID NO: 3, for example, 50 to 650, 50 to 600, 50 to 550, 50 to 500, 50 to 450, 50 to 400, 50 to 350, 50 to 300, 50 to 250, 50 to 200, 50 to 150, 50 to 100, 75 to 700, 75 to 650, 75 to 600, 75 to 550, 75 to 500, 75 to 450, 75 to 400, 75 to 350, 75 to 300, 75 to 250, 75 to 200, 75 to 150, 75 to 100, 100 to 700, 100 to 650, 100 to 600, 100 to 550, 100 to 500, 100 to 450, 100 to 400, 100 to 350, 100 to 300, 100 to 250, 100 to 200, 100 to 150, 200 to 700, 200 to 650, 200 to 600, 200 to 550, 200 to 500, 200 to 450, 200 to 400, 200 to 350, 200 to 300, 200 to 250, 300 to 700, 300 to 650, 300 to 600, 300 to 550, 300 to 500, 300 to 450, 300 to 400, 300 to 350, 400 to 700, 400 to 650, 400 to 600, 400 to 550, 400 to 500, 400 to 450, 500 to 700, 500 to 650, 500 to 600, 500 to 550, 600 to 700, or 600 to 650 contiguous nucleotides of SEQ ID NO: 3. In some examples, the TOMT regulatory element includes about 50 to about 1300 contiguous nucleotides of SEQ ID NO: 4, for example, for example, 50 to 1200, 50 to 1100, 50 to 1000, 50 to 1000, 50 to 950, 50 to 900, 50 to 850, 50 to 800, 50 to 750, 50 to 700, 50 to 650, 50 to 600, 50 to 550, 50 to 500, 50 to 450, 50 to 400, 50 to 350, 50 to 300, 50 to 250, 50 to 200, 50 to 150, 50 to 100, 75 to 1300, 75 to 1200, 75 to 1100, 75 to 1000, 75 to 950, 75 to 900, 75 to 850, 75 to 800, 75 to 750, 75 to 700, 75 to 650, 75 to 600, 75 to 550, 75 to 500, 75 to 450, 75 to 400, 75 to 350, 75 to 300, 75 to 250, 75 to 200, 75 to 150, 75 to 100, 100 to 1300, 100 to 1200, 100 to 1100, 100 to 1100, 100 to 1000, 100 to 950, 100 to 900, 100 to 850, 100 to 800, 100 to 750, 100 to 700, 100 to 650, 100 to 600, 100 to 550, 100 to 500, 100 to 450, 100 to 400, 100 to 350, 100 to 300, 100 to 250, 100 to 200, 100 to 150, 75 to 1300, 75 to 1200, 200 to 1100, 200 to 1000, 200 to 950, 200 to 900, 200 to 850, 200 to 800, 200 to 750, 200 to 700, 200 to 650, 200 to 600, 200 to 550, 200 to8123-110315-03500, 200 to 450, 200 to 400, 200 to 350, 200 to 300, 200 to 250, 300 to 1300, 300 to 1200, 300 to 1100, 300 to 1000, 300 to 950, 300 to 900, 300 to 850, 300 to 800, 300 to 750, 300 to 700, 300 to 650, 300 to 600, 300 to 550, 300 to 500, 300 to 450, 300 to 400, 300 to 350, 400 to 1300, 400 to 1200, 400 to 1100, 400 to 1000, 400 to 950, 400 to 900, 400 to 850, 400 to 800, 400 to 750, 400 to 700, 400 to 650, 400 to 600, 400 to 550, 400 to 500, 400 to 450, 500 to 1300, 500 to 1200, 500 to 1100, 500 to 1000, 500 to 950, 500 to 900, 500 to 850, 500 to 800, 500 to 750, 500 to 700, 500 to 650, 500 to 600, 500 to 550, 600 to 1300, 600 to 1200, 600 to 1100, 600 to 1000, 600 to 950, 600 to 900, 600 to 850, 600 to 800, 600 to 750, 600 to 700, 600 to 650, 700 to 1300, 700 to 1200, 700 to 1100, 700 to 1000, 700 to 950, 700 to 900, 700 to 850, 700 to 800, 700 to 750, 800 to 1300, 800 to 1200, 800 to 1100, 800 to 1000, 800 to 950, 800 to 900, 800 to 850, 900 to 1300, 900 to 1200, 900 to 1100, 900 to 1000, 900 to 950, 950 to 1100, 950 to 1000, 1000 to 1300, 1000 to 1200, 1000 to 1100, 1100 to 1300, 1100 to 1200, or 1200 to 1300 contiguous nucleotides of SEQ ID NO: 4. In some examples, the TOMT regulatory element includes about 50 to about 75 contiguous nucleotides of SEQ ID NO: 5, for example, 50 to 70, 50 to 65, 50 to 60, 50 to 55, 55 to 75, 55 to 70, 55 to 65, 55 to 60, 60 to 75, 60 to 70, 60 to 65, 65 to 75, or 65 to 70 contiguous nucleotides of SEQ ID NO: 5. In some examples, the TOMT regulatory element includes about 50 to about 500 contiguous nucleotides of SEQ ID NO: 6, for example, 50 to 400, 50 to 350, 50 to 300, 50 to 250, 50 to 200, 50 to 150, 50 to 100, 75 to 500, 75 to 450, 75 to 400, 75 to 350, 75 to 300, 75 to 250, 75 to 200, 75 to 150, 75 to 100, 100 to 500, 100 to 450, 100 to 400, 100 to 350, 100 to 300, 100 to 250, 100 to 200, 100 to 150, 200 to 500, 200 to 450, 200 to 400, 200 to 350, 200 to 300, or 200 to 250 contiguous nucleotides of SEQ ID NO: 6. In some examples, the TOMT regulatory element includes about 50 to about 1000 contiguous nucleotides of SEQ ID NO: 7, for example, 50 to 950, 50 to 900, 50 to 850, 50 to 800, 50 to 750, 50 to 700, 50 to 650, 50 to 600, 50 to 550, 50 to 500, 50 to 450, 50 to 400, 50 to 350, 50 to 300, 50 to 250, 50 to 200, 50 to 150, 50 to 100, 75 to 1000, 75 to 950, 75 to 900, 75 to 850, 75 to 800, 75 to 750, 75 to 700, 75 to 650, 75 to 550, 75 to 500, 75 to 450, 75 to 400, 75 to 350, 75 to 300, 75 to 250, 75 to 200, 75 to 150, 75 to 100, 100 to 1000, 100 to 950, 100 to 900, 100 to 850, 100 to 800, 100 to 750, 100 to 700, 100 to 650, 100 to 600, 100 to 550, 100 to 500, 100 to 450, 100 to 400, 100 to 350, 100 to 300, 100 to 250, 100 to 200, 100 to 150, 200 to 1000, 200 to 950, 200 to 900, 200 to 850, 200 to 800, 200 to 750, 200 to 700, 200 to 650, 200 to 600, 200 to 550, 200 to 500, 200 to 450, 200 to 400, 200 to 350, 200 to 300, 200 to 250, 300 to 1000, 300 to 950, 300 to 900, 300 to 850, 300 to 800, 300 to 750, 300 to 700, 300 to 650, 300 to 600, 300 to 550, 300 to 500, 300 to 450, 300 to 400, 300 to 350, 400 to 1000, 400 to 950, 400 to 900, 400 to 850, 400 to 800, 400 to 750, 400 to 700, 400 to 650, 400 to 600, 400 to 550, 400 to 500, 400 to 450, 500 to 1000, 500 to 950, 500 to 900, 500 to 850, 500 to 800, 500 to 750, 500 to 700, 500 to 650, 500 to 600, 500 to 550, 600 to 1000, 600 to 950, 600 to 900, 600 to 850, 600 to 800, 600 to 750, 600 to 700, 600 to 650, 700 to 1000, 700 to 950, 700 to 900, 700 to 850, 700 to 800, 700 to 750, 800 to 1000, 800 to 950, 800 to 900, 800 to 850, 900 to 1000, 900 to 950, or 950 to 1000 contiguous nucleotides of SEQ ID NO: 7. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 80% sequence identity, for example, at least 85%, at least 90%, at least 95%, at least 98%, at least 99%, or8123-110315-03more sequence identity to SEQ ID NO: 1. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 80% sequence identity, for example, at least 85%, at least 90%, at least 95%, at least 98%, at least 99%, or more sequence identity to SEQ ID NO: 2. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 80% sequence identity, for example, at least 85%, at least 90%, at least 95%, at least 98%, at least 99%, or more sequence identity to SEQ ID NO: 3. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 80% sequence identity, for example, at least 85%, at least 90%, at least 95%, at least 98%, at least 99%, or more sequence identity to SEQ ID NO: 4. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 80% sequence identity, for example, at least 85%, at least 90%, at least 95%, at least 98%, at least 99%, or more sequence identity to SEQ ID NO: 5. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 80% sequence identity, for example, at least 85%, at least 90%, at least 95%, at least 98%, at least 99%, or more sequence identity to SEQ ID NO: 6. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 80% sequence identity, for example, at least 85%, at least 90%, at least 95%, at least 98%, at least 99%, or more sequence identity to SEQ ID NO: 7. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 90% sequence identity to SEQ ID NO: 1. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 90% sequence identity to SEQ ID NO: 2. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 90% sequence identity to SEQ ID NO: 3. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 90% sequence identity to SEQ ID NO: 4. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 90% sequence identity to SEQ ID NO: 5. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 90% sequence identity to SEQ ID NO: 6. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 90% sequence identity to SEQ ID NO: 7. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 95% sequence identity to SEQ ID NO: 1. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 95% sequence identity to SEQ ID NO: 2. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 95% sequence identity to SEQ ID NO: 3. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 95% sequence identity to SEQ ID NO: 4. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 95% sequence identity to SEQ ID NO: 5. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 95% sequence identity to SEQ ID NO: 6. In some examples, the TOMT regulatory element includes a nucleic acid sequence having at least 95% sequence identity to SEQ ID NO: 7. In some examples, the TOMT regulatory element includes the nucleic acid sequence of SEQ ID NO: 1. In some examples, the TOMT regulatory element includes the nucleic acid sequence of SEQ ID NO: 2.8123-110315-03In some examples, the TOMT regulatory element includes the nucleic acid sequence of SEQ ID NO: 3. In some examples, the TOMT regulatory element includes the nucleic acid sequence of SEQ ID NO: 4. In some examples, the TOMT regulatory element includes the nucleic acid sequence of SEQ ID NO: 5. In some examples, the TOMT regulatory element includes the nucleic acid sequence of SEQ ID NO: 6. In some examples, the TOMT regulatory element includes the nucleic acid sequence of SEQ ID NO: 7. In some examples, the TOMT regulatory element consists of or essentially consists of the nucleic acid sequence of SEQ ID NO: 1. In some examples, the TOMT regulatory element consists of or essentially consists of the nucleic acid sequence of SEQ ID NO: 2. In some examples, the TOMT regulatory element consists of or essentially consists of the nucleic acid sequence of SEQ ID NO: 3. In some examples, the TOMT regulatory element consists of or essentially consists of the nucleic acid sequence of SEQ ID NO: 4. In some examples, the TOMT regulatory element consists of or essentially consists of the nucleic acid sequence of SEQ ID NO: 5. In some examples, the TOMT regulatory element consists of or essentially consists of the nucleic acid sequence of SEQ ID NO: 6. In some examples, the TOMT regulatory element consists of or essentially consists of the nucleic acid sequence of SEQ ID NO: 7. The disclosure includes functional variants of any of SEQ ID NOS: 1-7, which are sequence variants due to one or more mutations, such as nucleotide deletions, substitutions, additions, or combinations thereof, but retain promoter activity. In some examples, up to 5% (for example, up to 4%, up to 3%, up to 2%, or up to 1%) of the sequence includes deletions, substitutions, or additions. In some examples, the sequence of the TOMT regulatory element is optimized (e.g., the sequence is modified by deletions, substitutions, or additions) for expression in hair cells (e.g., cochlear and / or vestibular hair cells). The TOMT regulatory element is operably linked to a nucleic acid molecule such that the TOMT regulatory element induces expression of the nucleic acid molecule in inner ear hair cells (e.g., cochlear and / or vestibular hair cells). In some examples, the TOMT regulatory element is operably linked to a nucleic acid molecule such that the TOMT regulatory element induces expression of the nucleic acid molecule in cochlear hair cells. In some examples, expression is induced in both inner and outer hair cells of the cochlea. In some examples, the TOMT regulatory element is operably linked to a nucleic acid molecule such that the TOMT regulatory element induces expression of the nucleic acid molecule in vestibular hair cells. In some examples, expression is induced in both type I and type II hair cells of the vestibule. The nucleic acid molecule operably linked to the TOMT regulatory element can encode a product, such as a protein or RNA molecule. In some examples, the nucleic acid molecule encodes a gene associated with hearing loss and / or vestibular disorder, such as a gene provided in Table 2 or Table 3. Since symptoms of vestibular disorder are commonly experienced in subjects with genetic hearing loss, any of the genes listed in Table 2 may be useful for the treatment of hearing loss and / or vestibular disorders. Without being bound by any particular theory, underlying structural malformations or other defects of the inner ear may affect both hearing and vestibular function, resulting in the manifestation of both conditions. In some aspects, the nucleic acid is heterologous to the TOMT regulatory element such that the nucleic acid and TOMT regulatory element do not naturally occur together on a nucleic acid molecule.8123-110315-03Table 2: Exemplary hearing loss genes. Gene Hearing Chromosome NCBI References loss / Syndrome location Gene ID locus 19 8123-110315-03COL4A6 DFNX6 Xq22.3 1288 Rost et al., 2014 COL9A1 STL4 6q13 1297 Van Camp et al., 2006 l. ., 8123-110315-03KCNJ10 1q23.2 3766 Yang et al., 2009 KCNQ4 DFNA2A 1p34.2 9132 Kubisch et al., 1999 , 5 l., , 8123-110315-03POLR1C TCOF3 6p21.1 9533 Dauwerse et al., 2011 POLR1D TCOF2 13q12.2 51082 Dauwerse et al., 2011 ., , 8123-110315-03TRIOBP DFNB28 22q13.1 11078 Shahin et al., 2006; Riazuddin et al., 2006 TRRAP DFNA75 7q221 8295 Xia et al 2019 2; g loss. In some examples, the gene associated with hearing loss is a gene that is expressed in the cochlea. In some examples, the gene associated with hearing loss is a gene that is expressed in cochlear hair cells. In some examples, the hearing loss and / or vestibular disorder associated gene is ACTG1, ADCY1, ADGRV1 / VLGR1 / GPR98, AIFM1, ATP2B2, BDP1, BSND, CABP2, CCDC50, CD164, CDC14A, CDH23, CEACAM16, CHD7, CIB2, CLDN14, CLDN9, CLIC5, CLPP, CLRN1, CLRN2, COCH, COL11A1, COL11A2, COL2A1, COL4A3, COL4A4, COL4A5, COL4A6, COL9A1, COL9A2, CRYM, DCDC2, DIAPH1, DIAPH3, DMXL2, EDN3, EDNRB, ELMOD3, EPS8, EPS8L2, ERAL1, ESPN, ESRP1, ESRRB, EYA1, EYA4, FAM65B / RIPOR2, FOXI1, GAB1, GIPC3, GJB2, GJB3, GJB6, GPSM2, GRAP, GRHL2, GRXCR1, GRXCR2, GSDME, HARS1, HARS2, HGF, HOMER2, HSD17B4, IFNLR1, ILDR1, KARS1, KCNE1, KCNJ10, KCNQ4, KITLG, KCNQ1, LARS2, LHFPL5, LMX1A, LOXHD1, MAP1B, MARVELD2, MCM2, MET, METTL13, MIRN96, MITF, MPZL2, MSRB3, MYH14, MYH9, MYO15A, MYO3A, MYO6, MYO7A, NARS2, NDP, NLRP3, OSBPL2, OTOA, OTOF, OTOG, OTOGL, P2RX2, PAX3, PCDH15, PDE1C, PDZD7, PJVK, PLS1, PNPT1, POLR1C, POLR1D, POU3F4, POU4F3, PPIP5K2, PRPS1, PTPRQ, RDX, REST, ROR1, S1PR2, SANS / USH1G, SCD5, SEMA3E, SERPINB6, SIX1, SIX5, SLC12A2, SLC17A8, SLC22A4, SLC26A4, SLC26A5, DIABLO / SMAC, SMPX, SNAI2, SOX10, SPNS2, STRC, SYNE4, TBC1D24, TCOF1, TECTA, TJP2, TMC1, TMEM132E, TMIE, TMPRSS3, TNC, TOMT (LRTOMT / COMT), TPRN, TRIOBP, TRRAP, TSPEAR, TWNK, USH1C, USH2A, WBP2, WFS1, or WHRN. This disclosure contemplates any known isoforms or degenerate variants of the genes provided in Table 2. In some examples, the hearing loss gene is a human gene. In some examples, the hearing loss and / or vestibular disorder associated gene is CLRN1, CLRN2, HOMER2, LOXHD1, PJVK, SANS / USH1G, SYNE4, TMC1, TMIE, TMPRSS3, TOMT, WHRN, or USH1C. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or CLRN1. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or CLRN2. In some8123-110315-03examples, the hearing loss and / or vestibular disorder associated gene is TOMT or HOMER2. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or LOXHD1. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or PJVK. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or SANS / USH1G. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or SYNE4. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or TMC1. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or TMIE. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or TMPRSS3. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or WHRN. In some examples, the hearing loss and / or vestibular disorder associated gene is TOMT or USH1C. Although the genes listed in Table 2 are useful for the treatment of vestibular disorders, further, examples of genes associated with vestibular disorders are provided in Table 3. Table 3: Exemplary genes associated with vestibular disorders. Gene (OMIM) NCBI Gene ID Key Reference (Pubmed) PVRL3 25945 Hromatka et al 2015 8123-110315-03ATXN2 6311 Serrano-Munuera et al 2013 BEAN 146227 Sato et al 2009 vestibular disorder. In some examples, the gene associated with vestibular disorder is a gene that is expressed in the vestibule of the inner ear. In some examples, the gene associated with vestibular disorder is a gene that is expressed in vestibular hair cells. In a non-limiting example, the recombinant nucleic acid molecule includes a TOMT regulatory element and a nucleic acid encoding a heterologous TOMT gene (e.g., a TOMT coding sequence (CDS) or cDNA, or TOMT gene from another species (e.g., a Tomt regulatory element from mouse and a TOMT gene from human, or a TOMT regulatory element from human and an artificial TOMT gene)). The recombinant nucleic acid molecule is not naturally occurring, and thus excludes any naturally occurring nucleic acid molecules. In some examples, the TOMT gene is a human TOMT gene. In some examples, the TOMT gene is an artificial TOMT gene designed for expression in humans, for example, a non-human TOMT gene that is codon optimized for expression in humans. In some examples, the nucleic acid encoding the heterologous TOMT gene comprises a nucleic acid sequence encoding an amino acid sequence having at least 80% (e.g., at least 85%, 90%, 91%, 92%, 93%, 93%, 95%, 96%, 97%, 98%, 99%, or 100%) sequence identity to SEQ ID NO: 13 or SEQ ID NO: 15. In some examples, the nucleic acid encoding the heterologous TOMT gene comprises a nucleic acid sequence encoding an amino acid sequence having at least 95% sequence identity to SEQ ID NO: 13 or SEQ ID NO: 15. In some examples, the nucleic acid encoding the heterologous TOMT gene encodes the amino acid sequence of SEQ ID NO: 13 or SEQ ID NO: 15. In some examples, the TOMT gene is a CDS or cDNA sequence. In some examples, the TOMT gene has at least 80% sequence identity, for example, at least 85%, at least 90%, at least 95%, at least 98%, at least 99% or more, sequence identity to SEQ ID NO: 12 or SEQ ID NO: 14. In some examples, the TOMT gene has at least 90% sequence identity to SEQ ID NO: 12 or SEQ ID NO: 14. In some examples, the TOMT gene has at least 95% sequence identity to SEQ ID NO: 12 or SEQ ID NO: 14. In some examples, the TOMT gene has at least 98% sequence identity to SEQ ID NO: 12 or SEQ ID NO: 14. In some examples, the TOMT gene consists of or essentially consists of SEQ ID NO: 12, SEQ ID NO: 14, or a degenerate variant thereof. A degenerate variant refers to a nucleic acid sequence variant due to degeneracy8123-110315-03(redundancy) of the genetic code. While the nucleic acid sequence of degenerate variants differ, they encode the same amino acid sequence. Also disclosed are vectors including a recombinant nucleic acid molecule disclosed herein (e.g., the recombinant nucleic acid molecule including a TOMT regulatory element operably linked to a nucleic acid molecule). In some examples, the vector is a viral vector. Numerous suitable viral vectors are known, for example, retrovirus vectors, orthopox vectors, avipox vectors, fowlpox vectors, capripox vectors, suipox vectors, adenoviral vectors, adeno-associated viral vectors, herpes virus vectors, alpha virus vectors, baculovirus vectors, Sindbis virus vectors, vaccinia virus vectors, lentivirus vectors, poliovirus vectors, poxvirus vectors, highly attenuated vaccinia virus, baculovirus, and the like. In some examples, the vector is a retroviral vector, a lentiviral vector, an adenovirus vector, or an adeno-associated virus (AAV) vector. In some implementations, a disclosed recombinant nucleic acid is included in an adenoviral vector and / or adeno-associated viral (AAV) vector. AAV is not known to cause disease in humans and elicits a very mild immune response, and it can infect both dividing and quiescent cells and persist in an extrachromosomal state without integrating into the genome of the host cell. Because of these features, AAV vectors are suitable for the compositions and methods disclosed herein. The AAV vector can be any serotype, such as AAV1, AAV2, AAV3, AAV4, AAV5, AAV6, AAV7, AAV9, AAV10, AAV11, AAV12, PhP.eB, 2.7m8, DJ / 8, rh10, or AAV-PHP.S, or a hybrid of two or more AAV serotypes (such as, but not limited to AAV2 / 1, AAV2 / 7, AAV2 / 8 or AAV2 / 9). In some examples, a recombinant nucleic acid disclosed herein is included in an AAV2, AAV5, AAV6, AAV8, or AAV9 vector. In some examples, a recombinant nucleic acid disclosed herein is included in an AAV6 or AAV9 vector. In some examples, a recombinant nucleic acid disclosed herein is included in an PhP.eB vector. Methods of constructing vectors are described, for example, in Green and Sambrook, Molecular Cloning: A Laboratory Manual, 4th ed., Cold Spring Harbor Press, 2012. Similarly, construction and use of AAV vectors and AAV proteins of different serotypes have been described, for example, in Chao et al., Mol. Ther.2:619 (2000); Davidson et al., Proc. Natl. Acad. Sci. USA 97:3428 (2000); Xiao et al., J. Virol. 72:2224 (1998); Halbert et al., J. Virol.74:1524 (2000); Halbert et al., J. Virol.75:6615 (2001); and Auricchio et al., Hum. Molec. Genet.10:3075 (2001); any of which can be used to generate a vector disclosed herein. Alternatively, suitable AAV vectors can be obtained from academic, commercial, or public sources (e.g., the American Type Culture Collection, Manassas, Va.), or be synthetically produced based on sequences available in public databases (e.g., GenBank®). AAV virions that include mutations within the virion capsid may be used to infect particular cell types more effectively than non-mutated capsid virions. For example, suitable AAV mutants can include ligand insertion mutations to facilitate targeting of the AAV virion to specific cell types (e.g., cochlear hair cells). The construction and characterization of AAV capsid mutants including insertion mutants, alanine screening mutants, and epitope tag mutants is described, for example, in Wu et al., J. Virol.74:8635 (2000). Other AAV virions that can be used in methods described herein include capsid hybrids that are generated by molecular breeding of viruses as well as by exon shuffling. See, e.g., Soong et al., Nat. Genet., 25:4368123-110315-03(2000) and Kolman and Stemmer, Nat. Biotechnol.19:423 (2001). In some examples, the vector is modified to improve targeting to nervous system cells (e.g., PhP.eB or PhP.S, see Chan et al. Nature Neuroscience, 20:1172–1179 (2017)). Vectors optionally include regulatory elements, such as one or more enhancers, which are binding recognition sites for one or more transcription factors that increase transcription above that observed for a promoter alone. Procedures for producing vectors and cloning can be found, for example, in Green and Sambrook, Molecular Cloning: A Laboratory Manual, 4th ed., Cold Spring Harbor Press, 2012. In some aspects, the vector includes a gene encoding a selectable marker, for example and without limitation, a protein whose expression can be readily detected such as a fluorescent or luminescent protein or an enzyme that acts on a substrate to produce a colored, fluorescent, or luminescent substance ("detectable markers"). Exemplary detectable markers include fluorescent proteins, such as green fluorescent protein (GFP) blue, sapphire, yellow, red, orange, and cyan fluorescent proteins and variants thereof. Luminescent proteins such as luciferase (e.g., firefly or Renilla luciferase) are also exemplary detectable makers. In some examples, the selectable marker is a gene that encodes drug resistance or provides a function that can be used to purify cells, for example, neomycin resistance (neo), puromycin resistance (puro), guanine phosphoribosyl transferase (gpt), dihydrofolate reductase (DHFR), adenosine deaminase (ada), puromycin- N-acetyltransferase (PAC), hygromycin resistance (hyg), multidrug resistance (mdr), thymidine kinase (TK), hypoxanthine-guanine phosphoribosyltransferase (HPRT), or hisD. Also disclosed are pharmaceutical compositions including a recombinant nucleic acid disclosed herein (e.g., a nucleic acid including a TOMT regulatory element operably linked to a nucleic acid molecule) or a vector including the recombinant nucleic acid disclosed herein. The pharmaceutical composition can include a pharmaceutically acceptable carrier. In some examples, the recombinant nucleic acid or vector are in a lyophilized form for storage and suspended, for example in saline (e.g., 0.9% saline) or another suitable pharmaceutical carrier, when needed for administration. Suitable pharmaceutically acceptable carriers include, but are not limited to, liquids such as water, saline, glycerol, and ethanol. Pharmaceutically acceptable carriers can include pharmaceutical salts, for example, mineral acid salts such as hydrochlorides, hydrobromides, phosphates, sulfates, and the like; and the salts of organic acids such as acetates, propionates, malonates, benzoates, and the like. Pharmaceutically acceptable carriers can include auxiliary substances, such as wetting or emulsifying agents, stabilizing agents, pH buffering substances, and the like. A suitable carrier can be readily determined by a practitioner in view of the teachings here and other available sources of information, for example, a thorough discussion of pharmaceutically acceptable carriers / excipients is available in Remington’s Pharmaceutical Sciences, 23rd Edition, Academic Press, Elsevier, (2020). Pharmaceutical carriers can include additional excipients. In some examples, the pharmaceutical carrier confers a protective effect on the nucleic acids or vectors such that potential damage from formulation procedures, packaging, storage, transport, and the like, is minimized. In a specific, non-limiting example, the pharmaceutical carrier is considered "virion-stabilizing" in the sense that it provides higher8123-110315-03AAV virion titers and higher transduceability levels than a non-protected counterpart, as measured using standard assays. Such compositions therefore demonstrate increased transduceability levels as compared to compositions lacking protective excipients, and are therefore more stable than non-protected counterparts. Exemplary excipients that can be included in a pharmaceutically acceptable carrier that protect AAV vectors from degradative conditions include, but are not limited to, detergents, proteins (e.g., ovalbumin and bovine serum albumin), amino acids (e.g., glycine), polyhydric and dihydric alcohols, such as but not limited to polyethylene glycols (PEG) of varying molecular weights, such as PEG-200, PEG-400, PEG-600, PEG- 1000, PEG-1450, PEG-3350, PEG-6000, PEG-8000 and any molecular weights in between these values, with molecular weights of 1500 to 6000 preferred, propylene glycols (PG), and sugar alcohols, such as a carbohydrate, preferably, sorbitol. A detergent, when present, can be an anionic, a cationic, a zwitterionic, or a nonionic detergent. In some examples, the detergent is a nonionic detergent, such as a sorbitan ester, e.g., polyoxyethylenesorbitan monolaurate (TWEEN®-20) polyoxyethylenesorbitan monopalmitate (TWEEN®-40), polyoxyethylenesorbitan monostearate (TWEEN®-60), polyoxyethylenesorbitan tristearate (TWEEN®-65), polyoxyethylenesorbitan monooleate (TWEEN®-80), polyoxyethylenesorbitan trioleate (TWEEN®-85), such as TWEEN®-20 and / or TWEEN®-80. Protective excipients are commercially available from a number of vendors, such Sigma (St. Louis, Mo). The exact concentration of various excipients will vary, however, generally excipients are present at a concentration between 0.05 weight (wt) % to 20 weight (wt) %. In some examples a protein excipient, such as BSA, is present at a concentration of between 1.0 weight (wt) % to about 20 wt %, preferably 10 wt %. If an amino acid, e.g. glycine, is used in the formulation, it can be present at a concentration of about 1 wt. % to about 5 wt. %. A carbohydrate, e.g. sorbitol, if present, can be present at a concentration of about 0.1 wt % to about 10 wt. %, such as between about 0.5 wt. % to about 15 wt. %, or about 1 wt. % to about 5 wt. %. If polyethylene glycol is present, it can generally be present at about 2 wt. % to about 40 wt. %, such as about 10 wt. % top about 25 wt. %. If propylene glycol is used in the subject formulations, it will typically be present at a concentration of about 2 wt. % to about 60 wt. %, such as about 5 wt. % to about 30 wt. %. If a detergent, e.g. a sorbitan ester (TWEEN®), is present, it can be present at a concentration of about 0.05 wt. % to about 5 wt. %, such as between about 0.1 wt. % and about 1 wt %. In one example, an aqueous virion-stabilizing formulation comprises a carbohydrate, such as sorbitol, at a concentration of between 0.1 wt. % to about 10 wt. %, such as between about 1 wt. % to about 5 wt. %, and a detergent, such as a sorbitan ester (TWEEN®) at a concentration of between about 0.05 wt. % and about 5 wt. %, such as between about 0.1 wt. % and about 1 wt. %. In some examples, the pharmaceutically acceptable carrier includes or consists of about 0.1% to 2% saline, for example about 0.5%, about 0.7%, about 0.8%, about 9%, about 1%, or about 1.5% saline. In a non-limiting example, the pharmaceutically acceptable carrier includes or consists of about 0.9% saline. Virions are generally present in the composition in an amount sufficient to provide a therapeutic effect when given in one or more doses, as defined above. The pharmaceutical compositions can include a contrast dye. The contrast dye can be a low- osmolar low-viscosity non-ionic dye, a low-viscosity high-osmolar dye, or a dissociable high-viscosity dye.8123-110315-03In some examples, the contrast dye / stain is Fast Green FCF (also referred to as Food green 3 or FD&C Green No.3), a gadolinium-based contrast agent (e.g., gadodiamide (Omniscan®), gadobutrol (Gadovist®), gadobenate dimeglumine (MultiHance®), gadoterate meglumine (Dotarem®), gadopentetate dimeglumine (Magnograf® or Magnevist®)), or phalloidin-based contrast agent (e.g., phalloidin conjugated to a fluorescent dye, e.g., FITC, rhodamine, TRITC, or the like). In a specific non-limiting example, the contrast dye is Fast Green FCF. The pharmaceutical compositions including a disclosed recombinant nucleic acid or vector including the recombinant nucleic acid, are useful for gene therapy to treat hearing loss (e.g., genetic hearing loss) and / or vestibular disorders. In some examples, administering a pharmaceutical composition disclosed herein results in the expression of a nucleic acid molecule (e.g., gene associated with hearing loss and / or vestibular disorders, e.g., TOMT) in cochlear and / or vestibular hair cells of a subject (e.g., inner and / or outer hair cells or type I / II hair cells). In some aspects, the pharmaceutical compositions including a disclosed recombinant nucleic acid or vector including the recombinant nucleic acid, are useful for gene therapy to treat hearing loss (e.g., genetic hearing loss). In some aspects, administering a pharmaceutical composition disclosed herein results in the expression of a nucleic acid molecule (e.g., gene associated with hearing loss, e.g., TOMT) in cochlear hair cells of a subject (e.g., inner and / or outer hair cells). In some aspects, the pharmaceutical compositions including a disclosed recombinant nucleic acid or vector including the recombinant nucleic acid, are useful for gene therapy to treat vestibular disorders. In some examples, administering a pharmaceutical composition disclosed herein results in the expression of a nucleic acid molecule (e.g., gene associated with vestibular disorders, e.g., TOMT) in vestibular hair cells of a subject (e.g., type I and / or II hair cells). Further disclosed are host cells transformed with a recombinant nucleic acid disclosed herein or vector including the recombinant nucleic acid. Transformation includes any suitable method by which a recombinant nucleic acid molecule or vector disclosed herein is introduced into a cell, for example and without limitation, by chemical methods (e.g., calcium-phosphate transfection), physical methods (e.g., electroporation, microinjection, particle bombardment), fusion (e.g., liposomes), lipofection, nucleofection, receptor-mediated endocytosis (e.g., DNA-protein complexes, viral envelope / capsid-DNA complexes), biolistics (particle gun accelerator or gene gun), or other transduction and / or transfection methods. In a non- limiting example, transformation of a cell is achieved by transfection of a viral vector, such as an AAV vector including a TOMT regulatory element operably linked to a nucleic acid molecule (e.g., a gene associated with hearing loss and / or vestibular disorders, e.g., TOMT). A host cell can be transformed in vitro (e.g., cell culture) or in vivo (in an organism, such as a mouse). In some examples, the host cell excludes a transformed human cell that is in vivo. In some examples the host cell is an in vitro cell. The host cell can be prokaryotic or eukaryotic. In some examples, that host cell is a bacterial (e.g., E. coli), yeast (Saccharomyces cerevisiae), insect, plant, or mammalian cell (e.g., HEK293 or AAV-293). In some examples the host cell is a mammalian cell, such as a human, non-human primate, domestic dog, domestic cat, mouse, hamster, or rat cell. In some examples, the host cell is a human cell (e.g., HEK293 or8123-110315-03AAV-293). In some examples the host cell is a cell found in the inner ear, such as a cochlear hair cell. In some examples, the host cell is E. coli. A host cell transformed with a vector including a recombinant nucleic acid disclosed herein, such as an AAV vector, can be used to produce / manufacture the recombinant AAV virus virions, for example, for use in gene therapy. Such host cells can include genetic components for the production and / or packing of AAV vectors in the host cell, such as a rep gene, capsid protein, minigene, or other gene with helper function, under the control of inducible or constitutive promoters. In a specific, non-limiting example, the host cell is an HEK-293 or AAV-293 cell. AAV-293 cells are an HEK293 (human embryonic kidney cells) cell line optimized for packaging of AAV virions in a helper-free system. AAV-293 cells are transformed with three AAV helper-free system plasmids, which supply all of the trans-acting factors required for AAV replication and packaging in AAV-293 cells. Recombinant AAV viral virions prepared from infected AAV- 293 cells may be used to infect a variety of mammalian cells. In some examples, virions are isolated / purified from a host cell and used to prepare a pharmaceutical composition. In a non-limiting example of AAV production, a vector disclosed herein is co-transfected with a Rep-cap plasmid and helper plasmid encoding adenovirus genes (E4, E2A and VA) that mediate AAV replication into HEK293T packaging cells. After an incubation period, viral particles are harvested from cell lysate or supernatant depending on serotype and concentrated by PEG precipitation. For ultra-purified AAV (in vivo grade), viral particles are further purified and concentrated by cesium chloride (CsCl) gradient ultracentrifugation. AAV titers can be quantified by any suitable method, for example, by qPCR-based approaches. IV. Methods Also disclosed are methods of producing a heterologous protein in a host cell, including transforming the host cell with a vector disclosed herein, thereby producing the heterologous protein in the host cell. In some examples, the heterologous protein is a protein product of a hearing loss and / or vestibular disorder associated gene of Table 2 or Table 3. In some examples, the heterologous protein is TOMT (e.g., human TOMT). Further disclosed are methods of treating hearing loss and / or vestibular disorder in a subject, including administering to the subject a pharmaceutical composition disclosed herein (e.g., a pharmaceutical composition including a recombinant nucleic acid molecule including a TOMT regulatory element operably linked to a nucleic acid molecule, as disclosed herein). Administering the pharmaceutical composition treats genetic hearing loss and / or vestibular disorder in the subject. In some examples, a subject at risk of or having genetic hearing loss and / or vestibular disorder is selected for treatment. In some examples, the hearing loss is genetic hearing loss (hearing loss caused by genetics, e.g., a deleterious mutation in one or more genes listed in Table 2). The hearing loss can be sensorineural hearing loss or auditory neuropathy. In some examples, the hearing loss is nonsyndromic hearing loss. A subject at risk of developing hearing loss and / or vestibular disorder can be identified by known methods of screening, such as a genetic test to detect8123-110315-03the presence or absence of one or more mutations in a gene associated with hearing loss and / or vestibular disorder, such as a gene provided in Table 2 or Table 3. The TOMT regulatory element induces expression of the operably linked nucleic acid molecule specifically in cochlear hair cells of the subject (e.g., inner and / or outer hair cells), and thus has minimal potential for off-target effects and allows for specific targeting of cochlear hair cells regardless of the route of administration. In some implementations, the TOMT regulatory element does not induce expression of the operably linked nucleic acid molecule in neuronal cells. In some examples, the TOMT regulatory element is a promoter and / or enhancer. In some examples, the TOMT regulatory element is a promoter fragment. Exemplary suitable TOMT promoter fragments are disclosed herein (e.g., SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7). In some examples, the TOMT regulatory element includes a nucleic acid sequence of at least 50 (e.g., at least 75, at least 100, at least 250, at least 500, at least 750, at least 1000, at least 1500, at least 2000) contiguous nucleotides of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7, respectively. In some examples, the TOMT regulatory element includes or consists of a nucleic acid sequence having at least 80% (e.g., at least 85%, at least 90%, at least 95%, at least 98%, at least 99%, or more) sequence identity to SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7, respectively. In some examples, the TOMT regulatory element includes or consists of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7. In a non-limiting example, the TOMT regulatory element includes or consists of SEQ ID NO: 1. In a further non-limiting example, the TOMT regulatory element includes or consists of SEQ ID NO: 5. In another non-limiting example, the TOMT regulatory element includes or consists of SEQ ID NO: 6. In some examples, the nucleic acid molecule that is operably linked to the TOMT regulatory element encodes a gene associated with hearing loss and / or vestibular disorder, such as a gene provided in Table 2 or Table 3. In some examples, the hearing loss and / or vestibular disorder associated gene is ACTG1, ADCY1, ADGRV1 / VLGR1 / GPR98, AIFM1, ATP2B2, BDP1, BSND, CABP2, CCDC50, CD164, CDC14A, CDH23, CEACAM16, CHD7, CIB2, CLDN14, CLDN9, CLIC5, CLPP, CLRN1, CLRN2, COCH, COL11A1, COL11A2, COL2A1, COL4A3, COL4A4, COL4A5, COL4A6, COL9A1, COL9A2, CRYM, DCDC2, DIAPH1, DIAPH3, DMXL2, EDN3, EDNRB, ELMOD3, EPS8, EPS8L2, ERAL1, ESPN, ESRP1, ESRRB, EYA1, EYA4, FAM65B / RIPOR2, FOXI1, GAB1, GIPC3, GJB2, GJB3, GJB6, GPSM2, GRAP, GRHL2, GRXCR1, GRXCR2, GSDME, HARS1, HARS2, HGF, HOMER2, HSD17B4, IFNLR1, ILDR1, KARS1, KCNE1, KCNJ10, KCNQ4, KITLG, KCNQ1, LARS2, LHFPL5, LMX1A, LOXHD1, MAP1B, MARVELD2, MCM2, MET, METTL13, MIRN96, MITF, MPZL2, MSRB3, MYH14, MYH9, MYO15A, MYO3A, MYO6, MYO7A, NARS2, NDP, NLRP3, OSBPL2, OTOA, OTOF, OTOG, OTOGL, P2RX2, PAX3, PCDH15, PDE1C, PDZD7, PJVK, PLS1, PNPT1, POLR1C, POLR1D, POU3F4, POU4F3, PPIP5K2, PRPS1, PTPRQ, RDX, REST, ROR1, S1PR2, SANS / USH1G, SCD5, SEMA3E, SERPINB6, SIX1, SIX5, SLC12A2, SLC17A8, SLC22A4, SLC26A4, SLC26A5, DIABLO / SMAC, SMPX, SNAI2, SOX10, SPNS2, STRC, SYNE4, TBC1D24,8123-110315-03TCOF1, TECTA, TJP2, TMC1, TMEM132E, TMIE, TMPRSS3, TNC, TOMT (LRTOMT / COMT), TPRN, TRIOBP, TRRAP, TSPEAR, TWNK, USH1C, USH2A, WBP2, WFS1, or WHRN. In some examples, the hearing loss and / or vestibular disorder associated gene is a human gene. Expression of the gene associated with hearing loss and / or vestibular disorder in cochlear and / or vestibular hair cells (e.g., inner and / or outer hair cells or type I / II hair cells) increases an ability of the subject to perceive sound (improves hearing) and / or improves vestibular function (e.g., restores balance or sense of orientation, or improves another symptom of vestibular disorder). In some examples, the hearing loss and / or vestibular disorder-associated gene is TOMT (e.g., SEQ ID NO: 12 or SEQ ID NO: 14). In some aspects, a subject having a mutation or defect in one or more genes listed in Table 2 or Table 3 is selected for treatment. In some examples, a subject having a defect in one or more of: ACTG1, ADCY1, ADGRV1 / VLGR1 / GPR98, AIFM1, ATP2B2, BDP1, BSND, CABP2, CCDC50, CD164, CDC14A, CDH23, CEACAM16, CHD7, CIB2, CLDN14, CLDN9, CLIC5, CLPP, CLRN1, CLRN2, COCH, COL11A1, COL11A2, COL2A1, COL4A3, COL4A4, COL4A5, COL4A6, COL9A1, COL9A2, CRYM, DCDC2, DIAPH1, DIAPH3, DMXL2, EDN3, EDNRB, ELMOD3, EPS8, EPS8L2, ERAL1, ESPN, ESRP1, ESRRB, EYA1, EYA4, FAM65B / RIPOR2, FOXI1, GAB1, GIPC3, GJB2, GJB3, GJB6, GPSM2, GRAP, GRHL2, GRXCR1, GRXCR2, GSDME, HARS1, HARS2, HGF, HOMER2, HSD17B4, IFNLR1, ILDR1, KARS1, KCNE1, KCNJ10, KCNQ4, KITLG, KCNQ1, LARS2, LHFPL5, LMX1A, LOXHD1, MAP1B, MARVELD2, MCM2, MET, METTL13, MIRN96, MITF, MPZL2, MSRB3, MYH14, MYH9, MYO15A, MYO3A, MYO6, MYO7A, NARS2, NDP, NLRP3, OSBPL2, OTOA, OTOF, OTOG, OTOGL, P2RX2, PAX3, PCDH15, PDE1C, PDZD7, PJVK, PLS1, PNPT1, POLR1C, POLR1D, POU3F4, POU4F3, PPIP5K2, PRPS1, PTPRQ, RDX, REST, ROR1, S1PR2, SANS / USH1G, SCD5, SEMA3E, SERPINB6, SIX1, SIX5, SLC12A2, SLC17A8, SLC22A4, SLC26A4, SLC26A5, DIABLO / SMAC, SMPX, SNAI2, SOX10, SPNS2, STRC, SYNE4, TBC1D24, TCOF1, TECTA, TJP2, TMC1, TMEM132E, TMIE, TMPRSS3, TNC, TOMT (LRTOMT / COMT), TPRN, TRIOBP, TRRAP, TSPEAR, TWNK, USH1C, USH2A, WBP2, WFS1, or WHRN, is selected for treatment in the methods disclosed herein. In some examples, the nucleic acid molecule encodes a functional replacement of the one or more defective genes in the subject. In some examples, administering a pharmaceutical composition disclosed herein results in expression of a gene encoded by the nucleic acid molecule. The pharmaceutical compositions disclosed herein can be administered by any suitable route. In some examples, the pharmaceutical composition is administered orally, parenterally, topically, intranasally, by inhalation, intratympanic, canalostomy, cochleostomy, or systemically. Parenteral administration includes subcutaneous, intravenous, intramuscular, intraperitoneal, intrapleural, and intracisternal injections, or infusion techniques. In a non-limiting example, the pharmaceutical composition is administered topically or by a local injection (e.g., intratympanic). The administration route may vary, for example, based on the age or condition of the patient, and severity of the hearing loss and / or vestibular disorder. In some examples, the pharmaceutical composition is formulated for local delivery to the inner ear (e.g., administration into the perilymph or endolymph, through the oval window, round window, or horizontal8123-110315-03canal). In a non-limiting example, the pharmaceutical composition is formulated for local delivery to the inner ear through the posterior semicircular canal or round window. The exact dose of a pharmaceutical composition administered to a subject may vary depending on multiple factors, including the timing of administration, the subject being treated, the severity of the condition being treated, and the manner of administration. Generally, an appropriate dose is used that is sufficient to improve hearing or vestibular function without causing unwanted side effects. A unit dose need not be administered as a single administration (e.g., single injection) but may include continuous infusion over a set period of time. Dosing may be performed using a syringe pump to control infusion rate to minimize cellular damage, such as damage to the cochlea. In examples where the vector is an AAV vector (e.g., AAV1, AAV2, AAV3, AAV4, AAV5, AAV6, AAV7, AAV8, AAV9, AAV10, AAV11, AAV-PhP.eB, AAV-PhP.S, 2.7m8, DJ / 8, rh10), about 1×108to about 1×1015viral genomes (vg) are administered, for example, 1×108to 1×1015, 1×109to 1×1015, 1×1010to 1×1015, 1×1011to 1×1015, 1×1012to 1×1015, 1×1013to 1×1015, 1×1014to 1×1015, 1×108to 1×1014, 1×109to 1×1014, 1×1010to 1×1014, 1×1011to 1×1014, 1×1012to 1×1014, 1×1013to 1×1014, 1×108to 1×1013, 1×109to 1×1013, 1×1010to 1×1013, 1×1011to 1×1013, 1×1012to 1×1013, 1×108to 1×1012, 1×109to 1×1012, 1×1010to 1×1012, 1×108to 1×1011, 1×109to 1×1011, 1×1010to 1×1011, 1×108to 1×1010, 1×109to 1×1010, 1×108to 1×1019, vg are administered to the subject. In some examples, about 2×108, 3×108, 4×108, 5×108, 6×108, 7×108, 8×108, 9×108, 2×109, 3×109, 4×109, 5×109, 6×109, 7×109, 8×109, 9×109, 2×1010, 3×1010, 4×1010, 5×1010, 6×1010, 7×1010, 8×1010, 9×1010, 1×1011, 2×1011, 3×1011, 4×1011, 5×1011, 6×1011, 7×1011, 8×1011, 9×1011, 1×1012, 2×1012, 3×1012, 4×1012, 5×1012, 6×1012, 7×1012, 8×1012, 9×1012, 1×1013, 2×1013, 3×1013, 4×1013, 5×1013, 6×1013, 7×1013, 8×1013, 9×1013, 1×1014, 2×1014, 3×1014, 4×1014, 5×1014, 6×1014, 7×1014, 8×1014, or 9×1014vg are administered to the subject. Administration includes single or multiple administrations, for example, a pharmaceutical composition disclosed here can be administered once, or may be administered periodically until a therapeutic result is achieved or until side effects warrant discontinuation of therapy. In some examples, the pharmaceutical composition is administered once, twice, three times, four times, five times, six times, or more in the subject’s lifetime. In one example, the pharmaceutical composition is administered once to the subject. Additional treatments may be administered until a desired therapeutic effect is achieved. In some examples, the pharmaceutical composition is administered no more than 10 times, for example, no more than 9, no more than 8, no more than 7, no more than 6, no more than 5, no more than 4, no more than 3, or no more than 2 times in the subject’s lifetime. In some examples, a pharmaceutical composition disclosed herein is administered in an amount effective to decrease the severity of hearing loss in the subject (improve hearing). In some examples, the subject’s hearing is improved by at least 5%, at least 10%, at least 20%, at least 25%, at least 50%, at least 75%, at least 90%, at least 100%, at least 200%, at least 300%, at least 400%, or at least 500%, such as 5% to 500%, 5% to 400%, 5% to 300%, 5% to 200%, 5% to 100%, 5% to 75%, 5% to 50%, 10% to 400%, 10% to 300%, 10% to 200%, 10% to 100%, 10% to 75%, 10% to 50%, 25% to 400%, 25% to 300%, 25% to8123-110315-03200%, 25% to 100%, 25% to 75%, 25% to 50%, 50% to 400%, 50% to 300%, 50% to 200%, 50% to 100%, 50% to 75%, 100% to 400%, 100% to 300%, 100% to 200%, or 200% to 500%, as compared to a suitable control (such as an amount of hearing prior to the treatment). In some examples, the control is a measure of the subject’s hearing prior to administration of the pharmaceutical composition disclosed herein. A measurement of hearing can be quantitative (e.g., a clinical measurement) or qualitative (e.g., a patient’s self-reported perception of hearing). In some examples, administering a pharmaceutical composition disclosed herein restores the subject’s hearing to a clinically normal state. Hearing can be assessed using standard clinical tests, for example, audiometry, auditory brainstem response (ABR), electrocochleography(ECOG), or otoacoustic emissions (e.g., distortion product otoacoustic emissions (DPOAE)). In some examples, expression of a recombinant nucleic acid and / or vector disclosed herein does not cause toxicity in cochlear hair cells (e.g., clinically normal cochlear hair cells). Thresholds between 5- 20 dB are generally considered clinically normal. Standard clinical tests, for example, ABRs and DPOAEs, are useful for evaluating hair cell function and / or toxicity. Additional audiological tests and otologic exams can also be used to monitor hearing. In some examples, a subject’s hearing is monitored after administration of a pharmaceutical composition disclosed herein, and if the subject’s hearing is not clinically normal, a subsequent dose of the pharmaceutical composition is administered to the subject. In some examples, a pharmaceutical composition disclosed herein is administered in an amount effective to decrease the severity of vestibular disorder in the subject (e.g., improves vestibular function). In some examples, the subject’s vestibular function is improved by at least 5%, at least 10%, at least 20%, at least 25%, at least 50%, at least 75%, at least 90%, at least 100%, at least 200%, at least 300%, at least 400%, or at least 500%, such as 5% to 500%, 5% to 400%, 5% to 300%, 5% to 200%, 5% to 100%, 5% to 75%, 5% to 50%, 10% to 400%, 10% to 300%, 10% to 200%, 10% to 100%, 10% to 75%, 10% to 50%, 25% to 400%, 25% to 300%, 25% to 200%, 25% to 100%, 25% to 75%, 25% to 50%, 50% to 400%, 50% to 300%, 50% to 200%, 50% to 100%, 50% to 75%, 100% to 400%, 100% to 300%, 100% to 200%, or 200% to 500%, as compared to a suitable control (such as vestibular function prior to treatment). In some examples, the control is a measure of the subject’s vestibular function prior to administration of the pharmaceutical composition disclosed herein. A measurement of vestibular function can be quantitative (e.g., a clinical measurement) or qualitative (e.g., a patient’s self-reported perception of balance, orientation, or vertigo). In some examples, administering a pharmaceutical composition disclosed herein restores the subject’s vestibular function to a clinically normal state. Vestibular function can be assessed using known clinical tests and standards. In some examples, a pharmaceutical composition disclosed herein is administered in an amount effective to induce expression of the nucleic acid molecule in cochlear and / or vestibular hair cells of the subject (e.g., inner and / or outer hair cells, or type I / II hair cells). In some examples, a pharmaceutical composition disclosed herein is administered in an amount effective to induce expression of the nucleic acid molecule in cochlear hair cells (e.g., inner and / or outer hair cells). In some examples, a pharmaceutical composition disclosed herein is administered in an amount effective to induce expression of the nucleic acid8123-110315-03molecule in vestibular hair cells (e.g., type I and / or II hair cells). Expression can be evaluated using known techniques, such as immunohistochemistry, Western blot analysis, quantitative real-time PCR, or other methods for detecting protein or mRNA. In some examples, the nucleic acid molecule is a gene associated with hearing loss and / or vestibular disorder, such as a gene provided in Table 2 or Table 3. In a non-limiting example, the nucleic acid molecule is a TOMT gene that is heterologous to the TOMT regulatory element, and administering the pharmaceutical composition to the subject induces expression of the TOMT gene in cochlear and / or vestibular hair cells. In some examples, expression of the nucleic acid (e.g., TOMT) does not cause toxicity in cochlear and / or vestibular hair cells (e.g., clinically normal cochlear and / or vestibular hair cells). Following administration of the pharmaceutical composition, the subject can be evaluated for response to treatment, such as administering a hearing test (e.g,, audiometry, auditory brainstem response (ABR), electrocochleography (ECOG), or otoacoustic emissions) or balance tests, or by measuring expression of a gene encoded by the heterologous nucleic acid molecule (e.g., a gene from Table 2, e.g., TOMT) in cochlear and / or vestibular hair cells. V. Kits Also disclosed are kits including a recombinant nucleic acid, vector, or pharmaceutical composition disclosed herein. In some examples, the recombinant nucleic acid or vector are lyophilized. The kit can include a buffer or pharmaceutical carrier, for example to suspend a lyophilized recombinant nucleic acid or vector. In some examples, the kit includes a contrast agent or marker, for example, Fast Green FCF, a gadolinium-based contrast agent (e.g., gadodiamide (Omniscan®), gadobutrol (Gadovist®), gadobenate dimeglumine (MultiHance®), gadoterate meglumine (Dotarem®), gadopentetate dimeglumine (Magnograf® or Magnevist®)), phalloidin conjugated to a fluorescent dye (e.g., FITC, rhodamine, TRITC, AlexaFluor® 488 or iFluor 488), or DAPI. In some examples, the kit includes host cells, for example, HEK293, AAV-293, or E. coli. Kit components can be included in a single container, or multiple containers (e.g., individual containers for each component). The kits are of use in the methods disclosed herein. In some examples, the kits include written instructions (e.g., manual) for performing a method disclosed herein. Clauses I Clause 1. A recombinant nucleic acid molecule comprising a transmembrane-O-methyltransferase (TOMT) regulatory element operably linked to a nucleic acid molecule. Clause 2. The recombinant nucleic acid molecule of clause 1, wherein the TOMT regulatory element comprises: (i) SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7; (ii) a nucleic acid sequence comprising at least 80% sequence identity to SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7, respectively; or (iii) a nucleic acid sequence comprising at least 50 contiguous nucleotides of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7, respectively. Clause 3. The recombinant nucleic acid molecule of clause 2, wherein the TOMT regulatory element consists of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7.8123-110315-03Clause 4. The recombinant nucleic acid molecule of clause 3, wherein the TOMT regulatory element consists of SEQ ID NO: 1. Clause 5. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the nucleic acid molecule encodes a protein or RNA molecule. Clause 6. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the nucleic acid molecule encodes a gene associated with hearing loss. Clause 7. The recombinant nucleic acid molecule of clause 6, wherein the gene associated with hearing loss is ACTG1, ADCY1, ADGRV1 / VLGR1 / GPR98, AIFM1, ATP2B2, BDP1, BSND, CABP2, CCDC50, CD164, CDC14A, CDH23, CEACAM16, CHD7, CIB2, CLDN14, CLDN9, CLIC5, CLPP, CLRN1, CLRN2, COCH, COL11A1, COL11A2, COL2A1, COL4A3, COL4A4, COL4A5, COL4A6, COL9A1, COL9A2, CRYM, DCDC2, DIAPH1, DIAPH3, DMXL2, EDN3, EDNRB, ELMOD3, EPS8, EPS8L2, ERAL1, ESPN, ESRP1, ESRRB, EYA1, EYA4, FAM65B / RIPOR2, FOXI1, GAB1, GIPC3, GJB2, GJB3, GJB6, GPSM2, GRAP, GRHL2, GRXCR1, GRXCR2, GSDME, HARS1, HARS2, HGF, HOMER2, HSD17B4, IFNLR1, ILDR1, KARS1, KCNE1, KCNJ10, KCNQ4, KITLG, KCNQ1, LARS2, LHFPL5, LMX1A, LOXHD1, MAP1B, MARVELD2, MCM2, MET, METTL13, MIRN96, MITF, MPZL2, MSRB3, MYH14, MYH9, MYO15A, MYO3A, MYO6, MYO7A, NARS2, NDP, NLRP3, OSBPL2, OTOA, OTOF, OTOG, OTOGL, P2RX2, PAX3, PCDH15, PDE1C, PDZD7, PJVK, PLS1, PNPT1, POLR1C, POLR1D, POU3F4, POU4F3, PPIP5K2, PRPS1, PTPRQ, RDX, REST, ROR1, S1PR2, SANS / USH1G, SCD5, SEMA3E, SERPINB6, SIX1, SIX5, SLC12A2, SLC17A8, SLC22A4, SLC26A4, SLC26A5, DIABLO / SMAC, SMPX, SNAI2, SOX10, SPNS2, STRC, SYNE4, TBC1D24, TCOF1, TECTA, TJP2, TMC1, TMEM132E, TMIE, TMPRSS3, TNC, TOMT, TPRN, TRIOBP, TRRAP, TSPEAR, TWNK, USH1C, USH2A, WBP2, WFS1, or WHRN. Clause 8. The recombinant nucleic acid molecule of clause 6, wherein the gene associated with hearing loss is TOMT. Clause 9. A vector comprising the recombinant nucleic acid molecule of any one of clauses 1 to 8. Clause 10. The vector of clause 9, wherein the vector is a viral vector. Clause 11. The vector of clause 10, wherein the viral vector is a lentivirus vector, an adenovirus (AV) vector, or an adeno-associated virus (AAV) vector. Clause 12. The vector of clause 11, wherein the viral vector is the AAV vector. Clause 13. A host cell transformed with the recombinant nucleic acid molecule of any one of clauses 1 to 8, or the vector of any one of clause 9 to 12. Clause 14. A method of producing a heterologous protein in a host cell, comprising: transforming the host cell with the vector of any one of clauses 9 to 12, thereby producing the heterologous protein in the host cell. Clause 15. The host cell of clause 13 or method of clause 14, wherein the host cell is a cochlear hair cell. Clause 16. The host cell of clause 13 or method of clause 14, wherein the host cell is a mammalian cell. Clause 17. The host cell of clause 13 or method of clause 14, wherein the host cell is a human cell.8123-110315-03Clause 18. A pharmaceutical composition comprising the recombinant nucleic acid molecule of any one of clauses 1 to 8, or the vector of any one of clauses 9 to 12, and a pharmaceutically acceptable carrier. Clause 19. A method of treating hearing loss in a mammalian subject, comprising: administering an effective amount of the pharmaceutical composition of clause 18 to the subject, thereby treating hearing loss. Clause 20. The method of clause 19, wherein the TOMT regulatory element is operably linked to a gene associated with hearing loss. Clause 21. The method of clause 20, wherein the gene associated with hearing loss is TOMT. Clause 22. The method of any one of clauses 19 to 21, comprising administering an effective amount of the pharmaceutical composition comprising the vector. Clause 23. The method of any one of clauses 19 to 22, wherein the subject is a human. Clauses II Clause 1. A recombinant nucleic acid molecule comprising a transmembrane-O-methyltransferase (TOMT) regulatory element operably linked to a nucleic acid molecule. Clause 2. The recombinant nucleic acid molecule of clause 1, wherein the TOMT regulatory element comprises: (i) SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7; (ii) a nucleic acid sequence comprising at least 80% sequence identity to SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7, respectively; or (iii) a nucleic acid sequence comprising at least 50 contiguous nucleotides of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7, respectively. Clause 3. The recombinant nucleic acid molecule of clause 2, wherein the TOMT regulatory element consists of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7. Clause 4. The recombinant nucleic acid molecule of clause 3, wherein the TOMT regulatory element consists of SEQ ID NO: 1, 5, or 6. Clause 5. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the nucleic acid molecule encodes a protein or RNA molecule. Clause 6. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the nucleic acid molecule encodes a gene associated with hearing loss. Clause 7. The recombinant nucleic acid molecule of clause 6, wherein the gene associated with hearing loss is ACTG1, ADCY1, ADGRV1 / VLGR1 / GPR98, AIFM1, ATP2B2, BDP1, BSND, CABP2, CCDC50, CD164, CDC14A, CDH23, CEACAM16, CHD7, CIB2, CLDN14, CLDN9, CLIC5, CLPP, CLRN1, CLRN2, COCH, COL11A1, COL11A2, COL2A1, COL4A3, COL4A4, COL4A5, COL4A6, COL9A1, COL9A2, CRYM, DCDC2, DIAPH1, DIAPH3, DMXL2, EDN3, EDNRB, ELMOD3, EPS8, EPS8L2, ERAL1, ESPN, ESRP1, ESRRB, EYA1, EYA4, FAM65B / RIPOR2, FOXI1, GAB1, GIPC3, GJB2, GJB3, GJB6, GPSM2, GRAP, GRHL2, GRXCR1, GRXCR2, GSDME, HARS1, HARS2, HGF, HOMER2, HSD17B4, IFNLR1, ILDR1, KARS1, KCNE1, KCNJ10, KCNQ4, KITLG, KCNQ1, LARS2, LHFPL5, LMX1A, LOXHD1, MAP1B, MARVELD2, MCM2, MET, METTL13, MIRN96, MITF, MPZL2, MSRB3, MYH14, MYH9, MYO15A, MYO3A, MYO6, MYO7A, NARS2, NDP, NLRP3, OSBPL2, OTOA, OTOF, OTOG, OTOGL, P2RX2, PAX3, PCDH15, PDE1C, PDZD7, PJVK, PLS1, PNPT1, POLR1C, POLR1D,8123-110315-03POU3F4, POU4F3, PPIP5K2, PRPS1, PTPRQ, RDX, REST, ROR1, S1PR2, SANS / USH1G, SCD5, SEMA3E, SERPINB6, SIX1, SIX5, SLC12A2, SLC17A8, SLC22A4, SLC26A4, SLC26A5, DIABLO / SMAC, SMPX, SNAI2, SOX10, SPNS2, STRC, SYNE4, TBC1D24, TCOF1, TECTA, TJP2, TMC1, TMEM132E, TMIE, TMPRSS3, TNC, TOMT, TPRN, TRIOBP, TRRAP, TSPEAR, TWNK, USH1C, USH2A, WBP2, WFS1, or WHRN. Clause 8. The recombinant nucleic acid molecule of clause 6, wherein the gene associated with hearing loss is TOMT. Clause 9. A vector comprising the recombinant nucleic acid molecule of any one of clauses 1 to 8. Clause 10. The vector of clause 9, wherein the vector is a viral vector. Clause 11. The vector of clause 10, wherein the viral vector is a lentivirus vector, an adenovirus (AV) vector, or an adeno-associated virus (AAV) vector. Clause 12. The vector of clause 11, wherein the viral vector is the AAV vector. Clause 13. A host cell transformed with the recombinant nucleic acid molecule of any one of clauses 1 to 8, or the vector of any one of clauses 9 to 12. Clause 14. A method of producing a heterologous protein in a host cell, comprising: transforming the host cell with the vector of any one of clauses 9 to 12, thereby producing the heterologous protein in the host cell. Clause 15. The host cell of clause 13 or method of clause 14, wherein the host cell is a cochlear hair cell. Clause 16. The host cell of clause 13 or method of clause 14, wherein the host cell is a mammalian cell. Clause 17. The host cell of clause 13 or method of clause 14, wherein the host cell is a human cell. Clause 18. A pharmaceutical composition comprising the recombinant nucleic acid molecule of any one of clauses 1 to 8, or the vector of any one of clauses 9 to 12, and a pharmaceutically acceptable carrier. Clause 19. A method of treating hearing loss in a mammalian subject, comprising: administering an effective amount of the pharmaceutical composition of clause 18 to the subject, thereby treating hearing loss. Clause 20. The method of clause 19, wherein the TOMT regulatory element is operably linked to a gene associated with hearing loss. Clause 21. The method of clause 20, wherein the gene associated with hearing loss is TOMT. Clause 22. The method of any one of clauses 19 to 21, comprising administering an effective amount of the pharmaceutical composition comprising the vector. Clause 23. The method of any one of clauses 19 to 22, wherein the subject is a human. Clauses III Clause 1. A recombinant nucleic acid molecule comprising a transmembrane-O-methyltransferase (TOMT) regulatory element operably linked to a nucleic acid molecule. Clause 2. The recombinant nucleic acid molecule of clause 1, wherein the TOMT regulatory element comprises: (i) SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7; (ii) a nucleic acid sequence comprising at least 80% sequence identity to SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7, respectively; or (iii) a nucleic acid sequence comprising at least 50 contiguous nucleotides of SEQ ID NO: 1, 2, 3, 4, 5, 6, or 7, respectively.8123-110315-03Clause 3. The recombinant nucleic acid molecule of clause 1 or clause 2, wherein the TOMT regulatory element consists of: i) SEQ ID NO: 1; ii) SEQ ID NO: 2; iii) SEQ ID NO: 3; iv) SEQ ID NO: 4; v) SEQ ID NO: 5; vi) SEQ ID NO: 6; or vii) SEQ ID NO: 7. Clause 4. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the TOMT regulatory element comprises or consists of: i) SEQ ID NO: 1; ii) SEQ ID NO: 5; or iii) SEQ ID NO 6. Clause 5. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the nucleic acid molecule encodes a protein or RNA molecule. Clause 6. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the nucleic acid molecule encodes a gene associated with hearing loss and / or vestibular disorder. Clause 7. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the gene associated with hearing loss and / or vestibular disorder is ACTG1, ADCY1, ADGRV1 / VLGR1 / GPR98, AIFM1, ATP2B2, BDP1, BSND, CABP2, CCDC50, CD164, CDC14A, CDH23, CEACAM16, CHD7, CIB2, CLDN14, CLDN9, CLIC5, CLPP, CLRN1, CLRN2, COCH, COL11A1, COL11A2, COL2A1, COL4A3, COL4A4, COL4A5, COL4A6, COL9A1, COL9A2, CRYM, DCDC2, DIAPH1, DIAPH3, DMXL2, EDN3, EDNRB, ELMOD3, EPS8, EPS8L2, ERAL1, ESPN, ESRP1, ESRRB, EYA1, EYA4, FAM65B / RIPOR2, FOXI1, GAB1, GIPC3, GJB2, GJB3, GJB6, GPSM2, GRAP, GRHL2, GRXCR1, GRXCR2, GSDME, HARS1, HARS2, HGF, HOMER2, HSD17B4, IFNLR1, ILDR1, KARS1, KCNE1, KCNJ10, KCNQ4, KITLG, KCNQ1, LARS2, LHFPL5, LMX1A, LOXHD1, MAP1B, MARVELD2, MCM2, MET, METTL13, MIRN96, MITF, MPZL2, MSRB3, MYH14, MYH9, MYO15A, MYO3A, MYO6, MYO7A, NARS2, NDP, NLRP3, OSBPL2, OTOA, OTOF, OTOG, OTOGL, P2RX2, PAX3, PCDH15, PDE1C, PDZD7, PJVK, PLS1, PNPT1, POLR1C, POLR1D, POU3F4, POU4F3, PPIP5K2, PRPS1, PTPRQ, RDX, REST, ROR1, S1PR2, SANS / USH1G, SCD5, SEMA3E, SERPINB6, SIX1, SIX5, SLC12A2, SLC17A8, SLC22A4, SLC26A4, SLC26A5, DIABLO / SMAC, SMPX, SNAI2, SOX10, SPNS2, STRC, SYNE4, TBC1D24, TCOF1, TECTA, TJP2, TMC1, TMEM132E, TMIE, TMPRSS3, TNC, TOMT, TPRN, TRIOBP, TRRAP, TSPEAR, TWNK, USH1C, USH2A, WBP2, WFS1, or WHRN. Clause 8. The recombinant nucleic acid molecule of any one of the prior clauses, wherein the gene associated with hearing loss and / or vestibular disorder is TOMT. Clause 9. A vector comprising the recombinant nucleic acid molecule of any one of clauses 1 to 8. Clause 10. The vector of clause 9, wherein the vector is a viral vector. Clause 11. The vector of clause 9 or clause 10, wherein the viral vector is a lentivirus vector, an adenovirus (AV) vector, or an adeno-associated virus (AAV) vector. Clause 12. The vector of any one of clauses 9 to 11, wherein the viral vector is the AAV vector. Clause 13. A host cell transformed with the recombinant nucleic acid molecule of any one of clauses 1 to 8, or the vector of any one of clauses 9 to 12. Clause 14. A method of producing a heterologous protein in a host cell, comprising: transforming the host cell with the vector of any one of clauses 9 to 12, thereby producing the heterologous protein in the host cell. Clause 15. The host cell of clause 13 or method of clause 14, wherein the host cell is a cochlear hair cell.8123-110315-03Clause 16. The host cell of clause 13 or method of clause 14, wherein the host cell is a mammalian cell. Clause 17. The host cell of clause 13 or method of clause 14, wherein the host cell is a human cell. Clause 18. A pharmaceutical composition comprising the recombinant nucleic acid molecule of any one of clauses 1 to 8, or the vector of any one of clauses 9 to 12, and a pharmaceutically acceptable carrier. Clause 19. A method of treating hearing loss and / or vestibular disorder in a mammalian subject, comprising: administering an effective amount of the pharmaceutical composition of clause 18 to the subject, thereby treating hearing loss and / or vestibular disorder. Clause 20. The method of clause 19, wherein the TOMT regulatory element is operably linked to a gene associated with hearing loss and / or vestibular disorder. Clause 21. The method of clause 20, wherein the gene associated with hearing loss and / or vestibular disorder is TOMT. Clause 22. The method of any one of clauses 19 to 21, comprising administering an effective amount of the pharmaceutical composition comprising the vector. Clause 23. The method of any one of clauses 19 to 22, wherein the subject is a human. Clause 24. The method of any one of clauses 19 to 23, wherein the method treats hearing loss, and the TOMT regulatory element is operably linked to a gene associated with hearing loss. Clause 25. The method of any one of clauses 19 to 24, wherein the method treats vestibular disorder, and the TOMT regulatory element is operably linked to a gene associated with vestibular disorder. Clause 26. The method of any one of clauses 19 to 25, wherein the gene associated with hearing loss and / or vestibular disorder is expressed in inner ear hair cells of the subject following administration of the pharmaceutical composition. EXAMPLES The following examples are provided to illustrate particular features of certain aspects of the disclosure, but the scope of the claims should not be limited to those features exemplified. Example 1 Materials and Methods Gene regulatory fragment design: The mouse UCSC genome browser (GRCm38 / mm10) was used to identify regions of conservation (using Vertebrate Multiz Alignment & Conservation track) upstream of the predicted coding sequence for Tomt. Potential fragments were identified as areas with conservation across multiple mammalian species, including mice and humans. Fragments were designed to be around 1 kb. Potential fragments were cloned into an AAV expression vector. Posterior semicircular canal (PSCC) injections: Mice were anesthetized, a 2-3cm post-auricular incision made, tissue dissected and PSCC visualized. For neonatal mice, 2 μL of AAV vectors (serotype PHP.eB; viral titer >1x1013GC / ml) were delivered using a thinly pulled glass pipette with a microinjection apparatus8123-110315-03(Nanoject III®; 25nL / cycle, 10nL / sec, 80 cycles, and 10sec delay) For adults, dental etching gel (Metabond®) was applied for 1 min. to the PSCC surface to soften the bone, followed by surgical hole puncture with a 30G needle. A catheter comprised of 0.008” ID x 0.020” OD PE tubing, PE-10 tubing (Sci. Commodities), and pulled glass micropipette was fed into the PSCC and the hole sealed with surgical glue around the catheter. 2 μL of AAV vectors (serotype PHP.eB; viral titer >1x1013GC / ml) were delivered via Nanoject III® (25nL / cycle, 10nL / sec, 80 cycles, and 10sec delay). After delivery, the incision was closed with Vetbond™ (neonates) or a suture (adults). Mice were allowed to recover from anesthesia on a heating pad and returned to their home cage. Cloning (VectorBuilder): Vector cloning was performed using PCR-based and / or Gateway cloning. All vectors underwent stringent quality control to ensure that they contain the correct sequence exactly as designed. Common QC includes DNA quantification, A260 / 280 measurement, electrophoresis of undigested and restriction enzyme digested plasmid DNA, Sanger sequencing, recovering bacteria from glycerol stocks, and re-transformation. Viral production (VectorBuilder): For recombinant AAV manufacturing, an AAV transfer plasmid carrying the gene of interest (GOI) was co-transfected with VectorBuilder™ Rep-cap plasmid and helper plasmid encoding adenovirus genes (E4, E2A and VA) to mediate AAV replication into HEK293T packaging cells. After a short incubation period, viral particles were harvested from cell lysate or supernatant depending on serotype and concentrated by PEG precipitation. For ultra-purified AAV (in vivo grade), viral particles were further purified and concentrated by cesium chloride (CsCl) gradient ultracentrifugation. qPCR was used to measure AAV titer. Auditory brainstem response: Click and pure-tone ABR thresholds for mice were measured using a TDT RZ6 system as published (Cunningham et al 2017, 2020). Briefly, 4- to 8-week-old mice were anesthetized using Isoflurane and transferred into a sound-attenuation chamber while on a heating pad to maintain body temperature. An MF1 speaker was placed inside the external ear canal, and electrodes were inserted under the skin at the vertex and pinna while a ground was inserted under the skin near the tail. Click and Pure Tone stimuli were applied starting at an intensity of 90 dB and decreasing stepwise in intensity. Recordings were performed with a TDT System 6 auditory evoked response workstation (Tucker-Davis Technologies, Alachua, FL). Auditory thresholds were analyzed for both ears (for Click and Pure Tone) and for a range of frequencies (for Pure Tone, 8–32 kHz). ABR threshold is defined as the lowest stimulus intensity (in dB) which generates a waveform containing a reliable wave I. Immunohistochemistry: Whole mount and cryosectioned cochleas were dissected, fixed, and immunostained as previously described (Cunningham et al 2017, 2020). Briefly, temporal bones from mice are dissected away from the skull in 1x HBSS containing 1.5 mM CaCl2, and openings made in the bony cochlear shell at8123-110315-03the apex and through the oval and round windows. The temporal bones are incubated in 1x HBSS containing 4% PFA and 1.5 mM CaCl2 for 30 minutes at RT. The temporal bones are washed in 1x PBS, the bony cochlear shell removed, and the Organ of Corti separated from the modiolus and collected for immunostaining. Reissner’s membrane and the Tectorial membrane are removed, and the Organ of Corti is permeabilized in PBS containing 10% Donkey Serum (DS) and 0.5% Triton for 30 minutes at RT. After permeabilization, the tissue is blocked in PBS containing 10% DS for 1 hour. The tissue is incubated in PBS containing 10% DS and primary antibodies (see below) overnight at 4°C. The tissue was then washed three times in PBS, and incubated for 1-2 hours at RT in PBS containing 10% DS, secondary antibodies (1:2000-10000, Invitrogen, see below), Phalloidin conjugated to various AlexaFluor™ dyes (Invitrogen, Phalloidin 405 / 488 / 568 / 647, 1:200-500) and / or DAPI (1:10000, ThermoFisher). After secondary antibody incubation, the tissue was washed three times and mounted using on slides using ProLong™ Gold (Invitrogen). Whole mounts were imaged using 10x, 20x, 60x and 100x lenses on a Leica Stellaris 5 confocal microscope. Primary antibodies were as follows: Rabbit anti-Myosin VIIa (1:500, Proteus), Goat anti GFP (1:200, R&D Systems), Rabbit anti HA (1:500, CST), Goat anti HA (1:1000, Proteintech). Secondary antibodies were as follows: Donkey anti-Rabbit F(ab’)2 Alexa Fluor 555 (1: 5000, Invitrogen Superclonal), Donkey anti-Goat F(ab’)2 Alexa Fluor 647 (1:5000, Invitrogen). Example 2 TOMT Gene Therapy Targets Cochlear Hair Cells and Rescues Hearing The Tomt gene regulatory landscape (promoters, enhancers, etc.) is unknown, but Tomt mRNA and TOMT protein are expressed specifically in cochlear hair cells (FIGS.1A-1I). Additionally, Tomt expression begins earlier in development, and is expressed more robustly in both inner and outer hair cells than the other hair cell-specific promoters currently being utilized for gene therapy (e.g., Myo15). To advance Tomt gene therapy that targets only hair cells, the promoter region which drives hair- specific expression for Tomt was identified. To do this, regions of conservation across mammals (including humans) in the genomic region upstream of the mouse Tomt coding sequence were identified (FIG.2) and tested for their capacity for inner ear expression by incorporating into an AAV vector (serotype PhP.eB) and delivering locally to the inner ear using posterior semicircular canal injections. Initially, four putative Tomt promoter fragments were tested (SEQ ID NOs: 1-4, see FIGS.3A-3F and 7A-7C). Expression patterns were benchmarked and compared to multiple ubiquitous promoters (CMV, CAG, Ef1alpha) as well as a hair-cell-specific promoter (Myo15). One fragment (Tomt TV2 exon 1 fragment, SEQ ID NO: 1; see, FIGS. 3A-3F) was identified that (1) drives hair cell-type-specific expression in the cochlea, with very low expression in other cell types relative to ubiquitous promoters commonly used (e.g., CMV, CAG, etc); and (2) shows robust and comprehensive expression in both inner and outer hair cells throughout the tonotopic axis of the cochlea (from apex to base) relative to the ubiquitous promoters or Myo15. Other fragments were either not highly expressed in hair cells or exhibited variable expression in hair cells and other cell types (see, FIG.7A-7C).8123-110315-03To further improve the utility of the Tomt TV2 exon 1 promoter for AAV gene therapy, which has a limited carrying capacity, two shorter fragments of the Tomt TV2 exon 1 fragment were made based on predicted cell-type-specific promoter activity from inner ear CAGEseq and ATACseq data (see, FIG.2). These modified fragments were named Tomt TV2 Exon 1 CAGE (sometimes also referred to as TOMT TV2 CAGE; SEQ ID NO: 5) and Tomt TV2 Exon 1 CAGEATAC (sometimes also referred to as TOMT TV2 CAGEATAC; SEQ ID NO: 6). Tomt TV2 CAGEATAC was efficiently expressed in most inner and outer hair cells, along with some scattered nonsensory cells (see, FIG.4A and 4B). The specificity of commonly used promoters (CMV, Myo15, EF1alpha, and CAG) was assessed for cochlear hair cells in comparison to novel Tomt fragments. This was done by quantifying AAV PhP.eB- mediated GFP expression in vivo using whole mounts of the inner ear. Specifically, we measured the proportion of GFP+ cells driven by both commonly used and novel Tomt promoters that were MYO7A+ hair cells in cochlear whole mounts at P28 (FIG.4C-4D). It is important to note that cochlear whole mounts contain various cell types, including hair cells, support cells, and other nonsensory cells, but exclude spiral ganglion neurons. The number of GFP+ / MYO7A+ double-positive cells was compared to the total number of GFP+ cells. The analysis revealed that the Tomt promoters TV2 exon 1, CAGEATAC, and TV1 exon 1 + TV2 exon 1 were highly specific to hair cells, similar to the Myo15 promoter, whereas TV1 exon 1 alone and TV1 / TV2 exon 2 were not. Using cochlear cryosections, promoter activity in spiral ganglion neurons (SGNs), a key cochlear cell type that connects hair cells to the central auditory system, was explored. Notably, it was found that several ubiquitous promoters, along with the Myo15 promoter, were widely expressed in spiral ganglion neurons of the adult cochlea (FIGS.4E-4I). This was surprising, as Myo15 was previously thought to be specific to hair cells. In contrast, minimal expression of the Tomt fragments, TV2 exon 1 and TV2 exon 1 CAGEATAC, in spiral ganglion neurons was observed. These findings underscore the superior specificity of the novel Tomt promoters, even when compared to the Myo15 promoter, which was previously considered hair-cell-specific. The ability of the Tomt fragments to effectively rescue hearing in deaf mice was tested by local delivery of AAVs expressing Tomt driven by various fragments. Expression of wildtype Tomt to deaf Tomt mutant mice driven by Tomt TV2 exon 1 fragment or Tomt TV2 exon 1 CAGEATAC fragment significantly rescued hearing (FIG.5), as evidenced by significantly improved auditory brainstem response thresholds. Auditory brainstem response measurements allow for determining hearing thresholds in humans and mice. The rescue of Tomt TV2 exon 1 fragment was on par with the Myo15 promoter and better than ubiquitous promoters. Notably, the modified CAGEATAC fragment was superior over any other promoter, and restored hearing to normal hearing thresholds for click stimuli, and for the pure tone frequencies 8,12,16,20 kHz. These frequencies are those in the range of frequencies in mice that most overlap with human hearing frequencies. Thus, described herein are new hair-cell-specific promoter fragments that elicit robust hearing restoration in previously deaf mice. The restoration is better than any known promoter including Myo15 and ubiquitous promoters, and includes restoration to normal hearing thresholds at many different frequencies.8123-110315-03Importantly, both the Tomt TV2 exon 1 fragment and Tomt TV2 exon1 CAGEATAC fragment did not cause any hearing loss in wild-type mice (FIG.6), in contrast to ubiquitous promoters (e.g. CMV) and another hair-cell-specific promoter (e.g. Myo15). The cochleae of wild-type mice at P28 that had been injected with AAVs expressing Tomt, driven by commonly used promoters CMV and Myo15, as well as the novel promoters Tomt TV2 exon 1 and Tomt TV2 exon 1 CAGEATAC were examined (FIGS.8A-8F). The findings revealed that Tomt expression driven by the CMV and Myo15 promoters resulted in significant hair cell death in wild-type mice. In contrast, the Tomt TV2 exon 1 and Tomt TV2 exon 1 CAGEATAC promoters had no detrimental effects on hair cell survival. This is a key differentiating aspect of the TOMT promoters described herein, that offers an advantage for subsequent gene therapy applications. Together, the identification of new hair cell-type-specific promoters that elicit improved hearing rescue relative to other promoters, including hearing restoration equivalent to normal hearing levels in many frequencies without associated toxicity (hearing loss) is an important and unique advancement that opens the path for the development of cell-type-specific gene therapy approaches not only for Tomt-linked hearing loss but also for additional genes and gene mutations that cause deafness. Example 3 Treatment of Vestibular Disorders The inner ear also contains vestibular structures (saccule, utricle, and semicircular canals), which are essential for maintaining balance. Like the auditory system, vestibular structures rely on hair cells for their function, and genetic mutations that cause hearing loss often result in vestibular disorders as well. It was observed that Tomt mutant mice, which are profoundly deaf, also exhibit severe balance deficits, such as circling and head-tossing, indicative of vestibular dysfunction. Using an open field test (FIGS.9A-9B), these deficits were quantified and it was confirmed that Tomt mutant mice have significant vestibular impairments. To determine whether in vivo gene therapy could rescue vestibular behavior, various promoters driving Tomt expression, including Tomt TV2 exon 1 and Tomt TV2 exon 1 CAGEATAC, were tested. Through qualitative assessments of circling and head-tossing, it was found that almost all mice treated with gene therapy displayed no signs of these behaviors and behaved similarly to wild-type mice (FIGS.9B-9D). These results highlight the potential clinical utility of Tomt promoters in treating inner ear disorders affecting hair cells, including both hearing and vestibular dysfunctions. Overall, the identification of novel Tomt hair cell-specific promoters that enable superior hearing restoration compared to other promoters—achieving near-normal hearing levels across many frequencies without associated hair cell loss or toxicity—marks a significant advancement. This opens the door to cell- type-specific gene therapy approaches for Tomt-linked hearing loss and other genetic mutations that cause deafness. Furthermore, the successful in vivo rescue of vestibular function in Tomt mutant mice using these novel hair cell-specific promoters demonstrates their potential for also treating genetic vestibular disorders that impact hair cells.8123-110315-03Example 4 Gene Therapy Subjects with a deafness-causing gene mutation are administered a gene therapy pharmaceutical composition including a AAV PhP.eB vector carrying a transmembrane-O-methyltransferase (TOMT) regulatory element operably linked to the coding sequence of a complementary gene in a saline carrier. The pharmaceutical composition is administered to the subject by local inner ear injection through the semicircular canal or round window. In a further example, subjects with a deafness-causing mutation in TOMT are administered a gene therapy pharmaceutical composition including a AAV PhP.eB vector carrying a transmembrane-O- methyltransferase (TOMT) regulatory element operably linked to a functional, complementary TOMT gene. The pharmaceutical composition is administered to the subject by local inner ear injection through the semicircular canal or round window. In either example, the subject’s hearing can be periodically monitored after treatment with the gene therapy. A subject determined to be in further need of treatment (e.g., hearing is not within a clinically normal range) can be administered the gene therapy a second or subsequent time. In another example, a subject harboring a genetic mutation causing vestibular disorder is administered a gene therapy pharmaceutical composition including a AAV PhP.eB vector carrying a transmembrane-O-methyltransferase (TOMT) regulatory element operably linked to the coding sequence of a complementary gene in a saline carrier. The pharmaceutical composition is administered to the subject by local inner ear injection through the semicircular canal or round window. The subject’s vestibular function can be periodically monitored after treatment. A subject determined to be in further need of treatment (e.g., hearing is not within a clinically normal range) can be administered the gene therapy a second or subsequent time. It will be apparent that the precise details of the methods or compositions described herein may be varied or modified without departing from the spirit of the disclosure. We claim all such modifications and variations that fall within the scope and spirit of the claims below.

Claims

8123-110315-03We claim:

1. A recombinant nucleic acid molecule comprising a transmembrane-O-methyltransferase (TOMT) regulatory element operably linked to a nucleic acid molecule.

2. The recombinant nucleic acid molecule of claim 1, wherein the TOMT regulatory element comprises: (i) SEQ ID NO: 6, 1, 2, 3, 4, 5, or 7; (ii) a nucleic acid sequence comprising at least 80% sequence identity to SEQ ID NO: 6, 1, 2, 3, 4, 5, or 7, respectively; or (iii) a nucleic acid sequence comprising at least 50 contiguous nucleotides of SEQ ID NO: 6, 1, 2, 3, 4, 5, or 7, respectively.

3. The recombinant nucleic acid molecule of claim 2, wherein the TOMT regulatory element consists of: i) SEQ ID NO: 6; ii) SEQ ID NO: 1; iii) SEQ ID NO: 2; iv) SEQ ID NO: 3; v) SEQ ID NO: 4; vi) SEQ ID NO: 5; or vii) SEQ ID NO:

7.

4. The recombinant nucleic acid molecule of claim 3, wherein the TOMT regulatory element comprises or consists of: i) SEQ ID NO: 6; ii) SEQ ID NO: 1; or iii) SEQ ID NO 5.

5. The recombinant nucleic acid molecule of claim 1, wherein the nucleic acid molecule encodes a protein or RNA molecule.

6. The recombinant nucleic acid molecule of claim 1, wherein the nucleic acid molecule encodes a gene associated with hearing loss and / or vestibular disorder.

7. The recombinant nucleic acid molecule of claim 6, wherein the gene associated with hearing loss and / or vestibular disorder is TOMT, ACTG1, ADCY1, ADGRV1 / VLGR1 / GPR98, AIFM1, ATP2B2,8123-110315-03BDP1, BSND, CABP2, CCDC50, CD164, CDC14A, CDH23, CEACAM16, CHD7, CIB2, CLDN14, CLDN9, CLIC5, CLPP, CLRN1, CLRN2, COCH, COL11A1, COL11A2, COL2A1, COL4A3, COL4A4, COL4A5, COL4A6, COL9A1, COL9A2, CRYM, DCDC2, DIAPH1, DIAPH3, DMXL2, EDN3, EDNRB, ELMOD3, EPS8, EPS8L2, ERAL1, ESPN, ESRP1, ESRRB, EYA1, EYA4, FAM65B / RIPOR2, FOXI1, GAB1, GIPC3, GJB2, GJB3, GJB6, GPSM2, GRAP, GRHL2, GRXCR1, GRXCR2, GSDME, HARS1, HARS2, HGF, HOMER2, HSD17B4, IFNLR1, ILDR1, KARS1, KCNE1, KCNJ10, KCNQ4, KITLG, KCNQ1, LARS2, LHFPL5, LMX1A, LOXHD1, MAP1B, MARVELD2, MCM2, MET, METTL13, MIRN96, MITF, MPZL2, MSRB3, MYH14, MYH9, MYO15A, MYO3A, MYO6, MYO7A, NARS2, NDP, NLRP3, OSBPL2, OTOA, OTOF, OTOG, OTOGL, P2RX2, PAX3, PCDH15, PDE1C, PDZD7, PJVK, PLS1, PNPT1, POLR1C, POLR1D, POU3F4, POU4F3, PPIP5K2, PRPS1, PTPRQ, RDX, REST, ROR1, S1PR2, SANS / USH1G, SCD5, SEMA3E, SERPINB6, SIX1, SIX5, SLC12A2, SLC17A8, SLC22A4, SLC26A4, SLC26A5, DIABLO / SMAC, SMPX, SNAI2, SOX10, SPNS2, STRC, SYNE4, TBC1D24, TCOF1, TECTA, TJP2, TMC1, TMEM132E, TMIE, TMPRSS3, TNC, TPRN, TRIOBP, TRRAP, TSPEAR, TWNK, USH1C, USH2A, WBP2, WFS1, or WHRN.

8. The recombinant nucleic acid molecule of claim 7, wherein the gene associated with hearing loss and / or vestibular disorder is TOMT.

9. A vector comprising the recombinant nucleic acid molecule of claim 1.

10. The vector of claim 9, wherein the vector is a viral vector.

11. The vector of claim 10, wherein the viral vector is a lentivirus vector, an adenovirus (AV) vector, or an adeno-associated virus (AAV) vector.

12. The vector of claim 11, wherein the viral vector is the AAV vector.

13. A host cell transformed with the recombinant nucleic acid molecule of claim 1.

14. A method of producing a heterologous protein in a host cell, comprising: transforming the host cell with the vector of claim 9, thereby producing the heterologous protein in the host cell.

15. The host cell of claim 13 or method of claim 14, wherein the host cell is a cochlear hair cell.

16. The host cell of claim 13 or method of claim 14, wherein the host cell is a mammalian cell.8123-110315-0317. The host cell of claim 13 or method of claim 14, wherein the host cell is a human cell.

18. A pharmaceutical composition comprising the recombinant nucleic acid molecule of claim 1 and a pharmaceutically acceptable carrier.

19. A method of treating hearing loss and / or vestibular disorder in a mammalian subject, comprising: administering an effective amount of the pharmaceutical composition of claim 18 to the subject, thereby treating hearing loss and / or vestibular disorder.

20. The method of claim 19, wherein the TOMT regulatory element is operably linked to a gene associated with hearing loss and / or vestibular disorder.

21. The method of claim 20, wherein the gene associated with hearing loss and / or vestibular disorder is TOMT.

22. The method of claim 19, comprising administering an effective amount of the pharmaceutical composition comprising the vector.

23. The method of claim 19, wherein the subject is a human.

24. The method of claim 19, wherein the method treats hearing loss, and the TOMT regulatory operably linked to a gene associated with hearing loss.

25. The method of claim 19, wherein the method treats vestibular disorder, and the TOMT regulatory element is operably linked to a gene associated with vestibular disorder.

26. The method of claim 19, wherein the gene associated with hearing loss and / or vestibular disorder is expressed in inner ear hair cells of the subject following administration of the pharmaceutical composition.

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