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Genetic Mapping of a Light-Dependent Lesion Mimic Mutant Reveals the Function of Coproporphyrinogen III Oxidase Homolog in Soybean.

ABSTRACT: Lesion mimic mutants provide ideal genetic materials for elucidating the molecular mechanism of cell death and disease resistance. Here, we isolated a Glycine max lesion mimic mutant 2-1 (Gmlmm2-1), which displayed a light-dependent cell death phenotype. Map-based cloning revealed that GmLMM2 encods a coproporphyrinogen III oxidase and participates in tetrapyrrole biosynthesis. Knockout of GmLMM2 led to necrotic spots on developing leaves of CRISPR/Cas9 induced mutants. The GmLMM2 defect decreased the chlorophyll content by disrupting tetrapyrrole biosynthesis and enhanced resistance to Phytophthora sojae. These results suggested that GmLMM2 gene played an important role in the biosynthesis of tetrapyrrole and light-dependent defense in soybeans.

SUBMITTER: Ma J

PROVIDER: S-EPMC7227399 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Genetic Mapping of a Light-Dependent Lesion Mimic Mutant Reveals the Function of Coproporphyrinogen III Oxidase Homolog in Soybean.

Ma Jingjing J Yang Suxin S Wang Dongmei D Tang Kuanqiang K Feng Xing Xing XX Feng Xian Zhong XZ

Frontiers in plant science 20200508

Lesion mimic mutants provide ideal genetic materials for elucidating the molecular mechanism of cell death and disease resistance. Here, we isolated a Glycine max lesion mimic mutant 2-1 (Gmlmm2-1), which displayed a light-dependent cell death phenotype. Map-based cloning revealed that GmLMM2 encods a coproporphyrinogen III oxidase and participates in tetrapyrrole biosynthesis. Knockout of GmLMM2 led to necrotic spots on developing leaves of CRISPR/Cas9 induced mutant ...[more]

PMID: 32457787

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Project description:In plants, lesion mimic mutants (LMMs) reveal spontaneous disease-like lesions in the absence of pathogen that constitutes powerful genetic material to unravel genes underlying programmed cell death (PCD), particularly the hypersensitive response (HR). However, only a few LMMs are reported in soybean, and no related gene has been cloned until now. In the present study, we isolated a new LMM named spotted leaf-1 (spl-1) from NN1138-2 cultivar through ethyl methanesulfonate (EMS) treatment. The present study revealed that lesion formation might result from PCD and excessive reactive oxygen species (ROS) accumulation. The chlorophyll content was significantly reduced but antioxidant activities, viz., superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT), as well as the malondialdehyde (MDA) contents, were detected higher in spl-1 than in the wild-type. According to segregation analysis of mutant phenotype in two genetic populations, viz., W82×spl-1 and PI378692×spl-1, the spotted leaf phenotype of spl-1 is controlled by a single recessive gene named lm1. The lm1 locus governing mutant phenotype of spl-1 was first identified in 3.15 Mb genomic region on chromosome 04 through MutMap analysis, which was further verified and fine mapped by simple sequence repeat (SSR) marker-based genetic mapping. Genetic linkage analysis narrowed the genomic region (lm1 locus) for mutant phenotype to a physical distance of ~76.23 kb. By searching against the Phytozome database, eight annotated candidate genes were found within the lm1 region. qRT-PCR expression analysis revealed that, among these eight genes, only Glyma.04g242300 showed highly significant expression levels in wild-type relative to the spl-1 mutant. However, sequencing data of the CDS region showed no nucleotide difference between spl-1 and its wild type within the coding regions of these genes but might be in the non-coding regions such as 5' or 3' UTR. Hence, the data of the present study are in favor of Glyma.04g242300 being the possible candidate genes regulating the mutant phenotype of spl-1. However, further validation is needed to prove this function of the gene as well as its role in PCD, which in turn would be helpful to understand the mechanism and pathways involved in HR disease resistance of soybean.

Project description:Lesion mimics (LMs) that exhibit spontaneous disease-like lesions in the absence of pathogen attack might confer enhanced plant disease resistance to a wide range of pathogens. The LM mutant, lm3 was derived from a single naturally mutated individual in the F1 population of a 3-1/Jing411 cross, backcrossed six times with 3-1 as the recurrent parent and subsequently self-pollinated twice. The leaves of young seedlings of the lm3 mutant exhibited small, discrete white lesions under natural field conditions. The lesions first appeared at the leaf tips and subsequently expanded throughout the entire leaf blade to the leaf sheath. The lesions were initiated through light intensity and day length. Histochemical staining revealed that lesion formation might reflect programmed cell death (PCD) and abnormal accumulation of reactive oxygen species (ROS). The chlorophyll content in the mutant was significantly lower than that in wildtype, and the ratio of chlorophyll a/b was increased significantly in the mutant compared with wildtype, indicating that lm3 showed impairment of the biosynthesis or degradation of chlorophyll, and that Chlorophyll b was prone to damage during lesion formation. The lm3 mutant exhibited enhanced resistance to wheat powdery mildew fungus (Blumeria graminis f. sp. tritici; Bgt) infection, which was consistent with the increased expression of seven pathogenesis-related (PR) and two wheat chemically induced (WCI) genes involved in the defense-related reaction. Genetic analysis showed that the mutation was controlled through a single partially dominant gene, which was closely linked to Xbarc203 on chromosome 3BL; this gene was delimited to a 40 Mb region between SSR3B450.37 and SSR3B492.6 using a large derived segregating population and the available Chinese Spring chromosome 3B genome sequence. Taken together, our results provide information regarding the identification of a novel wheat LM gene, which will facilitate the additional fine-mapping and cloning of the gene to understand the mechanism underlying LM initiation and disease resistance in common wheat.

Dataset Information

Genetic Mapping of a Light-Dependent Lesion Mimic Mutant Reveals the Function of Coproporphyrinogen III Oxidase Homolog in Soybean.

Publications

Genetic Mapping of a Light-Dependent Lesion Mimic Mutant Reveals the Function of Coproporphyrinogen III Oxidase Homolog in Soybean.

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