Rice lesion-like mutant rsl1 and application thereof

Abstract

The invention discloses a rice lesion-like mutant rsl1 and application thereof. Belongs to the field of agricultural biotechnology. The rice lesion-like mutant rsl1 is a mutant of an RSL1 gene; the nucleotide sequence of the RSL1 gene is as shown in SEQ ID NO: 1, and the coded amino acid sequence is as shown in SEQ ID NO: 2; the mutation is that the translation of the RSL1 gene is terminated in advance due to the mutation of one or more basic groups. According to the invention, a lesion-like mutant is screened from an EMS mutagen library of a japonica rice variety Taibei 309, and the lesion-like mutant is named as rsl1. The research on the gene can further clarify the change of hormone in the plant after rice scabs are generated, and the gene has important significance and value for the research of a plant hormone regulation theory in the field of abiotic stress, and provides key theoretical support and technical guidance for the cultivation of a new rice variety which is adaptive to a complex environment and has high and stable yield.

Description

Technical Field

[0001] The invention relates to the field of agricultural biotechnology, and more particularly to a rice disease spot mutant rsl1 and an application thereof. Background Art

[0002] Rice lesion mimic (LM) refers to the spontaneous formation of necrotic spots of different sizes and colors on the leaves, sheaths, stems and other parts of rice without any biotic and abiotic stress. At present, the main factors for the formation of rice lesion mimic include excessive accumulation of reactive oxygen species, imbalance of plant hormones and disorder of material metabolic pathways. Among them, plant hormones play a vital role in plant growth, development, reproduction and response to environmental stress. Different hormones form a complex hormone regulation network through synergistic or antagonistic effects, and jointly regulate the physiological processes of plants and the formation of lesion mimics. However, the imbalance of plant hormones, especially the antagonism or synergistic imbalance of the signaling pathways of JA and SA, may cause symptoms similar to lesions on rice leaves. In addition, the abnormal increase of ABA levels may interfere with normal cell metabolism and growth processes, further aggravating the formation of lesion mimics. Rice can also improve its own disease resistance and alleviate various abiotic stresses such as salinity, drought, high temperature and low temperature due to the increase of hormone levels such as JA and SA. Phytohormones play crucial roles in plant responses to abiotic stresses.

[0003] The yield and quality of rice play a vital role in human development. Rice uses a series of sophisticated and complex physiological and molecular mechanisms to precisely regulate its response to abiotic stresses such as drought, high temperature, and salinity, thereby achieving dynamic adaptation to environmental changes. The appearance of rice lesions may lead to a disorder in the plant hormone regulatory system in rice. Therefore, studying the regulation of plant hormones under abiotic stresses in rice lesions and analyzing the physiological and molecular mechanisms of rice in response to adversity will help screen and cultivate new rice varieties that can effectively resist abiotic stresses and have high yields and good quality. This is of significant significance for rice breeding and ensuring my country's food security. Summary of the invention

[0004] In view of this, the present invention provides a rice lesion-like mutant rsl1 and its application. The lesions are rust-like in the early tillering stage and brown-red in the late maturity stage, which affects the growth and development of rice, changes its agronomic traits, and participates in exogenous plant response and abiotic stress, which is of great value for rice lesion-like disease research, growth and development mechanism research and breeding research.

[0005] In order to achieve the above object, the present invention adopts the following technical solution:

[0006] Rice lesion-like mutant rsl1,

[0007] The rice lesion-like mutant rsl1 is a mutant of the RSL1 gene (i.e., the LOC_Os07g10390 gene);

[0008] The nucleotide sequence of the RSL1 gene is shown in SEQ ID NO: 1, and the encoded amino acid sequence is shown in SEQ ID NO: 2;

[0009] The mutation is a mutation of one or several bases that causes the translation of the RSL1 gene to terminate prematurely.

[0010] Furthermore,

[0011] The mutant rsl1 is a mutation of the 1683rd base in the coding region of the RSL1 gene from C to A.

[0012] Furthermore,

[0013] The nucleotide sequence of the RSL1 gene of the mutant rsl1 is shown in SEQ ID NO:3, and the encoded amino acid sequence is shown in SEQ ID NO:4.

[0014] The application of the above-mentioned rice lesion-like mutant rsl1 in rice breeding.

[0015] Furthermore,

[0016] The mutant rsl1 showed reduced sensitivity to exogenous SA, ABA and IAA, but increased sensitivity to exogenous MeJA and GA.

[0017] Furthermore,

[0018] The mutant rsl1 had decreased tolerance to salt stress, alkali stress, drought stress and high temperature stress, but increased tolerance to cold stress.

[0019] The application of the rice lesion-like mutant rsl1 in preparing experimental materials for rice lesion-like research.

[0020] The application of the rice lesion-like mutant rsl1 in preparing experimental materials for studying the growth and development mechanism of rice.

[0021] It can be seen from the above technical solution that, compared with the prior art, the beneficial effects achieved by the present invention are:

[0022] The present invention screened a rust-like mutant from the EMS mutagenesis library of japonica rice variety Taipei 309, and named it rsl1 (rust spotted leaf 1). Research on it can further clarify the changes in hormones in plants after rice rusts are produced, which has important significance and value for the study of plant hormone regulation theory in the field of abiotic stress, and provides key theoretical support and technical guidance for the cultivation of new rice varieties that are adaptable to complex environments and have high and stable yields. BRIEF DESCRIPTION OF THE DRAWINGS

[0023] In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the drawings required for use in the embodiments or the description of the prior art will be briefly introduced below. Obviously, the drawings described below are only embodiments of the present invention. For ordinary technicians in this field, other drawings can be obtained based on the provided drawings without paying creative work.

[0024] Figure 1 This is a phenotypic analysis of the wild type (WT) and the mutant (rsl1) in Example 2 of the present invention, wherein A is a phenotypic diagram of WT and rsl1 at the peak tillering stage, with a scale of 6 cm; B is a phenotypic diagram of WT and rsl1 leaves at the early tillering stage, with a scale of 0.2 cm; C is a phenotypic diagram of WT and rsl1 leaves at the peak tillering stage, with a scale of 0.5 cm; D is a phenotypic diagram of WT and rsl1 leaves at the mature stage, with a scale of 4 cm;

[0025] Figure 2 is the linkage map of RSL1 on rice chromosome 7 in Example 4 of the present invention, wherein A is the initial location of RSL1; B to C are the fine location of RSL1 (ORFs open reading frames only list functional proteins); D is the gene structure of RSL1; E is the single base mutation site of RSL1; F is the amino acid change of RSL1;

[0026] Figure 3The effects of exogenous hormone treatment on the wild type (WT) and mutant (rsl1) in Example 5 of the present invention, wherein A is the phenotype of WT and rsl1 after MeJA treatment, and the scale is 1 cm; B is the plant height of WT and rsl1 after MeJA treatment; C is the root length of WT and rsl1 after MeJA treatment; D is the phenotype of WT and rsl1 after SA treatment, and the scale is 1 cm; E is the plant height of WT and rsl1 after SA treatment; F is the root length of WT and rsl1 after SA treatment; G is the phenotype of WT and rsl1 after ABA treatment, and the scale is The ruler is 1 cm; H is the plant height of WT and rsl1 after ABA treatment; I is the root length of WT and rsl1 after ABA treatment; J is the phenotype of WT and rsl1 after IAA treatment, the ruler is 2 cm; K is the plant height of WT and rsl1 after IAA treatment; L is the root length of WT and rsl1 after IAA treatment; M is the phenotype of WT and rsl1 after GA treatment, the ruler is 2 cm; N is the plant height of WT and rsl1 after GA treatment; O is the root length of WT and rsl1 after GA treatment; * represents P < 0.05; ** represents P < 0.01;

[0027] Figure 4 The abiotic stress phenotypes and related stress gene expression levels of the wild type (WT) and mutant (rsl1) in Example 6 of the present invention at the seedling stage; wherein A is the phenotype after 5 days of abiotic stress, and the scale is 2 cm; B is the phenotype after 5 days of stress recovery, and the scale is 2 cm; C is the survival rate after different stress treatments; D is the expression analysis of salt-tolerance-related salt-tolerance genes; E is the expression analysis of alkali-tolerance-related alkali-tolerance genes; F is the expression analysis of drought-tolerance-related drought-tolerance genes; G is the expression analysis of cold-tolerance-related cold-tolerance genes; H is the expression analysis of high-temperature-tolerance-related high-temperature-tolerance genes, * represents P<0.05; ** represents P<0.01;

[0028] Figure 5 It is the expression level of the plant hormone gene related to the wild type (WT) and the mutant (rsl1) under different stresses in Example 7 of the present invention, wherein A is the expression analysis of the relevant plant hormone before stress; B is the expression analysis of the relevant plant hormone after salt stress; C is the expression analysis of the relevant plant hormone after alkali stress; D is the expression analysis of the relevant plant hormone after drought stress; E is the expression analysis of the relevant plant hormone after high temperature stress; F is the expression analysis of the relevant plant hormone after cold stress, * represents P<0.05; ** represents P<0.01. DETAILED DESCRIPTION

[0029] The following will be combined with the drawings in the embodiments of the present invention to clearly and completely describe the technical solutions in the embodiments of the present invention. Obviously, the described embodiments are only part of the embodiments of the present invention, not all of the embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without creative work are within the scope of protection of the present invention.

[0030] The drugs required for the present invention are conventional experimental drugs, which are purchased from commercial channels; the experimental methods not mentioned are conventional experimental methods and will not be described in detail here.

[0031] Example 1

[0032] Acquisition of mutant materials

[0033] Chemical mutagenesis of japonica rice variety Taipei 309 by EMS:

[0034] Soak the seeds in clean water for 8 hours. Then drain the water and pour in the prepared 1% EMS solution to soak for 8 hours for mutagenesis. Stir with a small wooden stick several times to ensure uniform mixing. After mutagenesis, rinse the toxic EMS solution with running water, sow after germination at 25℃, transplant and harvest single plants, and manage the growth period according to normal field management. A disease spot mutant was obtained through screening and named rsl1.

[0035] The traits of the mutant have been stably inherited after multiple generations of self-pollination. All rice materials were planted in the experimental field of the College of Biochemistry of Zhejiang Normal University in Jinhua City, Zhejiang Province, and managed conventionally.

[0036] Example 2

[0037] Phenotypic analysis of plants

[0038] Under field conditions, compared with the wild type, rust-like spots appeared on the bottom leaves of the mutant rsl1 at the beginning of the tillering stage; at the peak of tillering, rust-like spots appeared on all leaves of the mutant rsl1, and the number of spots on the bottom leaves increased and began to wither; at the mature stage, the number of spots on the leaves of the mutant rsl1 gradually increased, making the leaves turn reddish brown as a whole ( Figure 1 ). At the same time, the plant height, ear length, number of primary branches, number of secondary branches, number of grains per ear and thousand-grain weight of the mutant were significantly lower than those of the wild type, and the grains of the mutant were significantly smaller than those of the wild type (Table 1).

[0039] Table 1 Comparison of main agronomic traits between wild type (WT) and mutant (rsl1)

[0040]

[0041] Note: * represents P<0.05; ** represents P<0.01.

[0042] Example 3

[0043] Population construction and genetic analysis

[0044] The mutant rsl1 was hybridized with TN1 and 9311, and the phenotypes of the F1 plants were normal, indicating that the mutant's trait was controlled by a recessive locus. The segregation ratio of the F2 segregation population was statistically analyzed (Table 2). The results showed that the segregation ratio of the normal phenotype plants and the mutant phenotype plants was close to 3:1 after the chi-square test, which was consistent with Mendel's law of gene segregation, indicating that the trait of rsl1 was controlled by a single recessive nuclear gene.

[0045] Table 2 Genetic analysis of lesion-like traits of mutant rsl1

[0046]

[0047]

[0048] Example 4

[0049] Fine mapping of the RSL1 gene

[0050] SSR primers were designed to be evenly distributed on the 12 chromosomes of rice, and polymorphism screening was performed on the mutants rsl1, TN1, and 9311. Then linkage analysis was performed using 21 F2 lesion-like plants to preliminarily confirm the chromosome location of the target gene. Genomic DNA was extracted using the CTAB method. The specific steps are as follows:

[0051] ① Weigh 0.1g of rice leaves and grind them into powder with liquid nitrogen, then add 500μL of DNA extraction buffer prepared with CTAB solution (2% (m / V) CTAB, 100mmol / L Tris-Cl, 20mmol / L EDTA, 1.4mol / L NaCl; pH 8.0), and incubate in a 65℃ water bath for 40 minutes. Add 500μL of chloroform:isoamyl alcohol (24:1 volume ratio) and mix well. Centrifuge at 10,000rpm for 10 minutes and transfer the supernatant to a new centrifuge tube.

[0052] ②. Add 2 / 3 to 1 volume of pre-cooled (to 4°C) isopropanol to the supernatant obtained after centrifugation in step ① above, and gently mix until DNA is precipitated. Centrifuge at 13,000 rpm for 10 minutes and pour out the supernatant.

[0053] ③. Wash the DNA precipitate obtained in step ② above with 200 μL of 75% (volume concentration) ethanol.

[0054] ④. Dry the washed DNA and dissolve it in 100 μL TE buffer or pure water.

[0055] ⑤. The concentration of the DNA sample obtained in step ④ above was detected by UV spectrophotometry, and the integrity of the DNA was detected by 0.8% agarose gel electrophoresis. The complete and suitable DNA was used for PCR amplification, and the incomplete DNA was re-extracted until the complete DNA was obtained.

[0056] The PCR reaction system used a 10 μL system: 1 μL DNA template, 0.5 μL each of forward and reverse primers (10 μmol / L), 5 μL Taq enzyme, and ddH2O was added to make up to 10 μL.

[0057] The PCR amplification program was as follows: pre-denaturation at 94°C for 4 min; denaturation at 94°C for 30 s, annealing at 55°C-60°C for 30 s (the temperature varied with primers), extension at 72°C for 30 s, 35 cycles; and finally extension at 72°C for 10 min.

[0058] The PCR products were electrophoresed on a 4% agarose gel, and the gel was photographed and read using a gel imager. The 120 pairs of SSR primers screened above were used for linkage analysis of the RSL1 gene, and linkage was found at B7-7 and B7-9 on chromosome 7. New Indel markers were designed upstream and downstream of the linkage markers, and the target gene interval was locked between molecular markers M1 and M8 using the above 21 strains. New molecular markers were designed again in this interval, and 146 F2 strains were used to finally locate the gene in an interval of approximately 253.5 kb between M3 and M4 ( Figure 2 ). The primer sequences are shown in Table 3.

[0059] Table 3 Molecular markers used for fine mapping

[0060]

[0061] According to the data information of the rice genome database (http: / / rice.plantbiology.msu.edu / ), the accession number is LOC_Os07g10390, indicating that this gene is a candidate gene. The DNA of the wild type and the mutant was amplified using primers covering the gene region. The sequencing results showed that there was a C to A mutation in the 1683rd base of the coding region of the 8th exon of the RSL1 gene, which caused the protein to change from cysteine ​​to a stop codon (such as Figure 2 ).

[0062] The cDNA sequence of the RSL1 gene in Taipei 309 is shown in SEQ ID NO:1, and the amino acid sequence is shown in SEQ ID NO:2.

[0063] The 1683rd base in the coding region of the RSL1 gene in the rice disease spot mutant mutated from C to A, and the cDNA sequence after the mutation is shown in SEQ ID NO:3, resulting in a change in the structure of the protein encoded by it, and the amino acid sequence after the mutation is shown in SEQ ID NO:4.

[0064] The base substitution on the RSL1 gene obtained by the present invention causes the phenotype of reddish brown spots appearing on leaves, stems and grains of rice plants.

[0065]

[0066] MQGHPRLIFCLDDGEFHLLEFSLDMEGVKVLPECVHRGLPCKPLLWMDKGMVVGFVEMGDGMILQLENNRLVHKSAIQNVAPILDLAIADHHGEKQDQMFACCGMCPEGSLRVIRNGVNVEKLLRTDPIYHGVTGLWTLRMKRTDAYHSFLVLSFVEETRILSVGLSFNDICDAVGFQTDVCTLACGLVADGLLVQIHSKCVKLCLPTACAHPEGTLLPSPVCADWYPDVTISVGAVGHNVVVVATSNPCCLYILGVRSLSSFQYELYEIQHVQLHYEVSCISIPQEDWRLDNSSSSCATSGDFRKDFAANIRKFAVIGTHEPSVHIISLEPGEAFQQLAVGHISVNNALGTPISGCIPENVRFVAAARFYILAGLRNGMLLRFESQTSKGHCFPGSFYKESSTPCDDTSLMLIAVRRIGITPVVLVPLHDRANADIIVLGDRPWLLQSARHSLAYSSISFLPASHVTPVSSTDCPSGLLFVSENCLHLVEMVHGKRLNAQKFSIGGTPRKVLYHSDSRTLLVLRTGLTSVSCSSDIVQIDPSNGALLSRFKCEPGETAKCMQIAKIGNDQVLIVGTSKSNGRPMMPNGEAESIKGRLILLSLETIESPRESGSFTAASNLNSSHAGSPFPEFVGYAAEELSSNSMCSSPDEVCCNQIQPELMAGHLRSLVQHTFNGAVLAVHPYLDRYVLAAAGNVLFVFGFLNESPHRIKKYTTSRTRFTITCLKTYASRIAVGDCRDGVLFYSYHENLRKLELIYSDPAQRLVGDVALLSCETAVVSDRRGSISVLSCPRLEVSESPEKNLAVHCSFYMGETAMSIQKVAFKHWLPIDDLTEPVLESVYNCVVASTLLGSIFVMIPLTSEEHQMLQDVQERLSVHPLTAPLLGNDHAEFRRRGIPSGVPPILDGDMLVQFLELTSEQQHDVLNIVSPGKKRQHDISVFQVMRALERVHYALN*,SEQ ID NO:2。

[0067]

[0068] *, SEQ ID NO:4.

[0069] Example 5

[0070] Exogenous plant hormone treatment

[0071] The mature seeds of wild type and mutant rsl1 were mechanically shelled, disinfected with 70% alcohol solution for 2 minutes and then with 30% sodium hypochlorite solution for 30 minutes, washed with sterile water and inoculated on 1 / 2MS medium containing 0.5μmol / L and 5.0μmol / L MeJA, 0.5mmol / L and 1.0mmol / L SA, 0.1μmol / L and 0.3μmol / L ABA, 0.5μmol / L and 1.0μmol / L IAA and 0.1μmol / L and 1.0μmol / L GA, respectively, and cultured in an artificial climate incubator for 7 days, and then the root length and plant height were counted. The results are shown in Figure 2. Figure 3As shown in the figure, under no hormone treatment, the plant height and root length of rsl1 were 82% and 144% of the wild type, respectively. When the ABA concentration was 0.1μmol / L and 0.3μmol / L, the plant height of rsl1 was 150% and 130% of the wild type, and the root length was 134% and 152%, respectively. Therefore, the application of exogenous ABA had no obvious inhibitory effect on the plant height growth of rsl1, and the application of exogenous SA had the same situation. The application of exogenous IAA promoted plant height and inhibited root length. Under different concentrations of IAA, the plant height and root length of rsl1 were about 80% and 110% of the wild type, respectively. The application of exogenous MeJA and GA had a significant inhibitory effect on the roots of rsl1. When the concentrations of MeJA and GA were 0.5μmol / L and 1.0μmol / L, respectively, the root length of rsl1 was 88% and 66% of the wild type, respectively. Compared with the wild type, rsl1 is insensitive to SA, ABA and IAA, but sensitive to MeJA and GA.

[0072] Example 6

[0073] Abiotic stress experiments

[0074] The wild type and rsl1 seedlings were selected for salt stress (175mmol / L NaCl), alkali stress (100mmol / L NaHCO3), drought stress (20% PEG-6000), cold stress (6℃) and high temperature stress (42℃). The phenotype was obvious after 5 days of treatment, and then they were transferred to normal nutrient solution for recovery culture. The survival rate of the wild type and mutants before and after treatment, the expression of related genes and the expression of their own genes (primers used are shown in Table 4) were measured. The results are shown in Table 4. Figure 4 shown.

[0075] The plant height of rice was inhibited to varying degrees after different stress treatments, among which cold stress had the most obvious inhibitory effect on rice plant height. In addition, the survival rate of the mutant rsl1 after salt stress, alkali stress, drought stress and high temperature stress was much lower than that of the wild type, but the survival rate after cold stress was 41%, higher than the 18% of the wild type. Quantitative results showed that the expression levels of rsl1 and different stress-related genes changed before and after stress, so it was speculated that rsl1 was involved in the response to salt stress, alkali stress, drought stress, cold stress and high temperature stress.

[0076] Example 7

[0077] Quantitative analysis of related plant hormone genes

[0078] In order to analyze whether RSL1 is involved in the expression regulation of plant hormone-related genes under salt stress (175 mmol / L NaCl), alkali stress (100 mmol / L NaHCO3), drought stress (20% PEG-6000), cold stress (6°C) and high temperature stress (42°C), the present invention used the qRT-PCR method to perform expression analysis on the related genes of these pathways.

[0079] RNA extraction was performed using the RNeasy Plant Mini Kit (QIAGEN) to isolate total RNA from leaf samples of the mutant and wild type at the tillering stage. The expression of each gene in the wild type and mutant was analyzed by real-time fluorescence quantitative PCR (qRT-PCR). OsActin was used as the internal reference gene, and 3 parallel wells were made for each reaction. -ΔΔCt Methods Relative quantitative analysis was performed, and the reaction was repeated three times. The real-time PCR instrument was 7500 real-time PCR system (Applied Biosystems, Life Technologies). The experimental data were statistically analyzed using Excel and SPSS19.0 software, and the differences between different data were compared using t-test.

[0080] The qRT-PCR reaction system (10 μL) was: 1 μL of cDNA template, 6 μL of SYBR qPCRMix (TOYOBO), 1 μL of each of forward and reverse primers (10 μmol / L), and ddH2O was added to 10 μL.

[0081] The qRT-PCR amplification program was as follows: 95°C for 30 s; 95°C for 5 s; 55°C for 10 s; 72°C for 15 s, for 40 cycles.

[0082] The required primers are shown in Table 4. Figure 5 shown.

[0083] The expression levels of different plant hormone-related genes under different stresses showed that the growth hormone-related genes OsAUX3, OsGH3.8, OsYUCCA1, and OsARF17 all showed a down-regulation or unchanged trend under salt stress, alkali stress, and cold stress, which may reduce the content of IAA in the plant and make the plant dwarf. Although they showed an up-regulation or unchanged trend under drought stress and high temperature stress, the reduced sensitivity of the mutant rsl1 to IAA may have caused the plant to become dwarfed. Under salt stress, the expression levels of DG1, OsRab16A, OsABA8ox2, and OsNCED1 in the mutant rsl1 decreased, reducing the ABA content in the body, resulting in a decrease in the expression of genes related to MeJA synthesis, and the salt tolerance of the mutant rsl1 was reduced. At the same time, although the expression level of OsGAE1 related to GA decreased, the expression levels of GA metabolism and transport related genes OsGA2ox3, OsSWEET3a and OsSLR1 decreased significantly, and the RSL1 mutation increased the sensitivity to GA. Therefore, compared with the wild type, the salt tolerance of the mutant rsl1 was reduced. Under alkaline stress, the expression levels of OsRab16A, OsABA8ox2 and OsNCED1 in the mutant rsl1 increased significantly, which can improve the K tolerance of rice seedlings under alkaline stress. + content, reducing Na + Content and Na + / K + ratio, improving alkali tolerance, but the survival rate of mutant rsl1 was reduced under alkali stress, which may be related to the insensitivity of mutant rsl1 to ABA. Although the MeJA synthesis-related genes OsJMT1, OsJar1, and OsJAR2 of mutant rsl1 were reduced under cold stress, its sensitivity to MeJA increased compared with the wild type, and the expression of OsGAE1 was close to zero, indicating that the GA level and signal transduction were low, which was conducive to the survival of mutants in cold-tolerant environments. Under drought stress, the expression of NPR1 in mutant rsl1 increased significantly, accelerating cell death. Under high temperature stress, the expression of RSL1 in mutant rsl1 was downregulated, and the expression of carotenoid cleavage dioxygenase (OsNCED1), as a key rate-limiting enzyme in the ABA biosynthesis pathway, was downregulated, which may reduce the heat tolerance of mutant rsl1.

[0084] Table 4 Primer sequences for real-time fluorescence quantitative PCR

[0085]

[0086]

[0087] The various embodiments in this specification are described in a progressive manner, and each embodiment focuses on the differences from other embodiments. The same or similar parts between the various embodiments can be referenced to each other.

[0088] The above description of the disclosed embodiments enables one skilled in the art to implement or use the present invention. Various modifications to these embodiments will be apparent to one skilled in the art, and the general principles defined herein may be implemented in other embodiments without departing from the spirit or scope of the present invention. Therefore, the present invention will not be limited to the embodiments shown herein, but rather to the widest scope consistent with the principles and novel features disclosed herein.

Claims

1. A rice lesion-like mutant rsl1, characterized in that: The rice lesion-like mutant rsl1 is a mutant of the RSL1 gene; The nucleotide sequence of the RSL1 gene is shown in SEQ ID NO: 1, and the encoded amino acid sequence is shown in SEQ ID NO: 2; The mutation is a mutation of one or several bases that causes the translation of the RSL1 gene to terminate prematurely.

2. The rice lesion-like mutant rsl1 according to claim 1, characterized in that The mutant rsl1 is a mutation of the 1683rd base in the coding region of the RSL1 gene from C to A.

3. The rice lesion-like mutant rsl1 according to claim 1, characterized in that The nucleotide sequence of the RSL1 gene of the mutant rsl1 is shown in SEQ ID NO:3, and the encoded amino acid sequence is shown in SEQ ID NO:

4.

4. Use of the rice lesion-like mutant rsl1 according to claim 1 in rice breeding.

5. The use according to claim 4, characterized in that The mutant rsl1 showed reduced sensitivity to exogenous SA, ABA and IAA, but increased sensitivity to exogenous MeJA and GA.

6. The use according to claim 4, characterized in that The mutant rsl1 had decreased tolerance to salt stress, alkali stress, drought stress and high temperature stress, but increased tolerance to cold stress.

7. Use of the rice lesion-like mutant rsl1 according to claim 1 in preparing experimental materials for rice lesion-like research.

8. Use of the rice lesion-like mutant rsl1 according to claim 1 in preparing experimental materials for studying the growth and development mechanism of rice.

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