47 results about "Deficient mutant" patented technology

The present invention relates to a nucleic acid molecule comprising the HpYPS1 gene encoding H. polymorpha yapsin1, a polypeptide encoded by the nucleic acid molecule, a H. polymorpha mutant strain having reduced yapsin activity by mutation of the HpYPS gene encoding H. polymorpha yapsin1, a recombinant H. polymorpha strain expressing a foreign protein produced by introducing a gene encoding the foreign protein into the H. polymorpha mutant strain, and a process for preparing a foreign protein comprising culturing the recombinant H. polymorpha strain under conditions to express the foreign protein and isolating the foreign protein from the culture.

The present invention relates to mutants of a parent Trichoderma strain, comprising a polynucleotide encoding a polypeptide and one or more (several) genes selected from the group consisting of a first subtilisin-like serine protease gene, a first aspartic protease gene, a trypsin-like serine protease gene, a second subtilisin-like serine protease gene, and a second aspartic protease gene, wherein the one or more (several) genes are modified rendering the mutant strain deficient in the production of one or more (several) enzymes selected from the group consisting of a first subtilisin-like serine protease, a first aspartic protease, a trypsin-like serine protease, a second subtilisin-like serine protease, and a second aspartic protease, respectively, compared to the parent Trichoderma strain when cultivated under identical conditions. The present invention also relates to methods of producing a polypeptide in such mutants and methods for producing such mutants.

The present invention relates to methods of producing a polypeptide, comprising: (a) cultivating a mutant of a parent Fusarium venenatum strain in a medium for the production of the polypeptide, wherein the mutant strain comprises a polynucleotide encoding the polypeptide and one or more (several) genes selected from the group consisting of pyrG, amyA, and alpA, wherein the one or more (several) genes are modified rendering the mutant strain deficient in the production of one or more (several) enzymes selected from the group consisting of orotidine-5′-monophosphate decarboxylase, alpha-amylase, and alkaline protease, respectively, compared to the parent Fusarium venenatum strain when cultivated under identical conditions; and (b) recovering the polypeptide from the cultivation medium. The present invention also relates to enzyme-deficient mutants of Fusarium venenatum strains and methods for producing such mutants.

This invention provides a rice gene coding beta-keto co A synthetase, OsKCS1, which comprises 2186bp and 1560bp coding zones at the upstream of the start codon with promoter function, codes 519 amino acid, and contains typical FAE1 CUT1 RppA domain. The function-deficient mutant P1424 obtained by inserting T-DNA into rice OsKCS1 gene has short plants, occasionally curled leaves, and low fruiting rate. Further research shows that the wax at the surfaces of the mutant gas-generating organs is obviously reduced, and the draught resistance is seriously influenced. The expression of OsKCS1 gene in the mutant can recover its wild phenotype, thus can confirm the direction relationship between OsKCS1 gene and synthesis and growth of wax on rice surfaces. The identification of the gene is important to research on synthesis of wax on rice surfaces, and breeding of draught-resistant rice or other monocotyledon crops.

The invention discloses a method for improving microalgae growth rate and oil yield, and the method includes the following steps: 1), after inoculation of microalgae, the microalgae is cultured for 2-5 days by continuous illumination or cycled illumination in a certain light and dark conditions at 20-35 DEG C and in the conditions of 20-200 mu mol photon in m<-2>s<-1>; 2), the microalgae strain obtained by the step 1) is inoculated again, and then cultured; and 3), the microalgae strain is cultured by step 1) as a training cycle, and then cultured by step 2) as a next training cycle, and the microalgae strain with the growth rate and oil yield both increased can be obtained by the cycled training. According to the method, the growth rate and oil yield both of wild microalgae strains and microalgae gene deficient mutants are increased, and compared with the large-scale screening, the method is less in workload and high in efficiency, is a new strain selection method, and has broad application prospects in microalgae biofuel development.

As the richest source of astaxanthin, a natural antioxidant and coloring agent, the unicellular green alga, Haematococcus pluvialis, is being commercially exploited. A major constraint in the Haematococcus production system, however, is the thick, rigid cell walls associated with astaxanthin-rich cysts (or aplanospores). The thick walls prevent the extraction of cellular materials and consequently reduce the bioavailability of astaxanthin. Using a physical, chemical, or enzymatic method to disrupt the cell wall has proven to be very expensive and also introduce the risk of oxidation of astaxanthin by atmospheric oxygen The present invention provides a novel method for solving this problem by introducing two genetically modified Haematococcus pluvialis mutants. These two mutants, named as D 13-17 and N54-22, contain remarkably reduced amounts of cell wall materials, but retain the growth potential and ability to accumulate astaxanthin as high as the wild type strain. Organic solvent extraction efficiency assay has demonstrated that cellular astaxanthin can be more effectively and efficiently extracted from the cell wall-deficient mutants than from the wild type, suggesting that the mutants may provide better bioavailability of astaxanthin to humans and animals. The said mutants can be used for production of natural astaxanthin for human and animal consumption

The present invention provides a method for manufacturing xylitol with high-yield and high-productivity by using a xylitol dehydrogenase-deficient mutant of xylitol producing microorganism. This goal is achieved through modification of the metabolic pathway of the xylitol producing microorganism, preferably a natural xylose-assimilating yeasts and fungi, by disrupting or inactivating the expression of desired genes.

The invention belongs to the technical field of goat molecular marker preparation, and in particular relates to three goat MC1R deficient mutants and application thereof. Three deficient mutants are found in a goat MC1R and application thereof, two mutation sites F250V and G255D casing receptor defects both are located in a sixth transmembrane domain, and another mutation site C267W casing the receptor defects is located on a third external loop. The alpha-MSH ligand affinity of the three MC1R deficient mutants is lost, inducible and constitutive cAMP levels are significantly reduced, and inducible and constitutive p-ERK are significantly reduced. The goat MC1R deficient mutants can lead to the fact that a melanin production signal is blocked and the formation of black coat is affected. The molecular marker can be applied to assisted marker selection of goat wool color.

The invention discloses two saccharose translocator ShSUT2 genes derived from sugarcane and application. According to the saccharose translocator genes ShSUT2A and ShSUT2B, amino acid sequences are respectively shown in SEQ ID NO 2 and 4, and base sequences of encoding genes ShSuT2A and ShSUT2B are respectively shown in SEQ ID NO 1 and 3. Absorbing function deficient mutant by yeast saccharose shows that the proteins encoded by ShSUT2A and ShSUT2B have saccharose transport activity. The ShSUT2A and ShSUT2B encoding genes are responsible for absorbing saccharose of apoplast in sugarcane plant and participate in transportation, distribution and accumulated physiological processes of sugarcane plant saccharose. The genes can provide new ways for improving transportation and distribution efficiency of sugarcane saccharose, promoting growth of the plant and improving sugarcane yields and sugar content.

The present invention relates to methods of producing a heterologous biological substance, comprising: (a) cultivating a mutant of a parent Aspergillus niger strain in a medium suitable for the production of the heterologous biological substance, wherein (i) the mutant strain comprises a first nucleotide sequence encoding the heterologous biological substance and one or more second nucleotide sequences comprising a modification of glaA and at least one of the genes selected from the group consisting of asa, amyA, amyB, prtT, and oah, and (ii) the mutant strain is deficient in the production of glucoamylase and at least one enzyme selected from the group consisting of acid stable alpha-amylase, neutral alpha-amylase A, and neutral alpha-amylase B, protease, and oxalic acid hydrolase compared to the parent Aspergillus niger strain when cultivated under identical conditions: and (b) recovering the heterologous biological substance from the cultivation medium. The present invention also relates to enzyme-deficient mutants of Aspergillus niger strains and methods for producing such mutants.

The present invention relates to a nucleic acid molecule comprising the HpYPS1 gene encoding H. polymorpha yapsin1, a polypeptide encoded by the nucleic acid molecule, a H. polymorpha mutant strain having reduced yapsin activity by mutation of the HpYPS gene encoding H. polymorpha yapsin1, a recombinant H. polymorpha strain expressing a foreign protein produced by introducing a gene encoding the foreign protein into the H. polymorpha mutant strain, and a process for preparing a foreign protein comprising culturing the recombinant H. polymorpha strain under conditions to express the foreign protein and isolating the foreign protein from the culture.

The present invention relates to methods of producing a polypeptide, comprising: (a) cultivating a mutant of a parent Fusarium venenatum strain in a medium for the production of the polypeptide, wherein the mutant strain comprises a polynucleotide encoding the polypeptide and one or more (several) genes selected from the group consisting of pyrG, amyA, and alpA, wherein the one or more (several) genes are modified rendering the mutant strain deficient in the production of one or more (several) enzymes selected from the group consisting of orotidine-5′-monophosphate decarboxylase, alpha-amylase, and alkaline protease, respectively, compared to the parent Fusarium venenatum strain when cultivated under identical conditions; and (b) recovering the polypeptide from the cultivation medium. The present invention also relates to enzyme-deficient mutants of Fusarium venenatum strains and methods for producing such mutants.

The present invention relates to methods of producing a heterologous biological substance, comprising: (a) cultivating a mutant of a parent Bacillus cell under conditions conducive for the production of the heterologous biological substance, wherein (i) the mutant cell comprises a first nucleic acid sequence directing synthesis of the heterologous biological substance and a second nucleic acid sequence comprising a modification of at least one of the genes cypX and yvmC, which are involved in the production of a red pigment, and (ii) the mutant cell is deficient in the production of the red pigment compared to the parent Bacillus cell when cultivated under the same conditions; and (b) recovering the heterologous biological substance from the cultivation medium. The present invention also relates to mutants of Bacillus cells and methods for producing the mutants.

The invention provides a sericin nerve guide, its preparation method and application. The sericin nerve conduit component provided by the present invention is sericin, and its preparation method comprises: using silkworm cocoons of a silk fibroin-deficient mutant variety Bombyx mori as raw material, pulverizing it and sterilizing it with ultraviolet light or ethanol, and then using LiBr or LiCl aqueous solution Carry out the extraction of sericin protein, and make the sericin protein aqueous solution with the concentration of 0.5~20wt% from the extract; For semi-finished catheters, the amount of covalent cross-linking agent used is to add 2-500 μL of covalent cross-linking agent with a concentration of 0.1-50 wt% per 1 ml of sericin aqueous solution; freeze-dry the semi-finished sericin nerve catheter to obtain sericin nerve guide. The sericin nerve conduit provided by the invention has good biological activity and biocompatibility, can be naturally degraded in vivo and can promote regeneration of long-distance injured peripheral nerves.

The invention relates to an application of a Zea mays grain transcription factor in the aspect of regulation and control of alcohal-soluble proteins. The factor comprises a base sequence shown in SEQ ID NO: 1. The protein ZmbZIP22 encoded by the sequence can be directly bonded to a 27kDa gamma-gliadin promoter and activate the 27kDa gamma-gliadin promoter. Gene-deficient mutant plants are obtained through carrying out Zea mays immature-embryo conversion by taking a gene fragment, shown in SEQ ID NO: 2, of ZmbZIP22 as a guide RNA by using a CRISPR-Cas9 technology. Compared with wild type grains, transgenic mutants have Zea mays grains with irregular and relative-thin protein body shells, the content of alcohal-soluble proteins in mature grains is remarkably lowered, the content of essential amino acids such as lysine, which are deficient to the conventional Zea mays, in the mature grains is remarkably increased, and thus, the nutritional quality of Zea mays is improved.

The invention discloses a method for regulating the salt tolerance of plants and salt-tolerance-related proteins. The invention provides a method for cultivating and regulating the salt-tolerance of plants, which includes regulating the expression of genes encoding salt-tolerance-related proteins in target plants, wherein , the salt-tolerance-related protein is a salt-tolerance-related protein from rice, the name is OsPRR73, and it is from rice Nipponbare. The present invention uses CRISPR / Cas9 technology to obtain OsPRR73 function-deficient mutants, performs 180mM NaCl simulated salt stress treatment, observes the phenotype and counts the survival rate after recovery treatment, and finally confirms that OsPRR73 plays a positive role in the process of responding to rice salt stress effect. The OsPRR73 of the present invention can be used as a salt tolerance gene and play an important role in rice salt resistance.

The invention provides lipid A deficient mutant Neisseria meningitidis cells, pharmaceutical compositions incorporating such cells, and methods of using such cells.