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<p>Lesion mimic mutants (LMMs) are ideal for dissecting plant immunity mechanisms.Here, we characterized <i>lm10373</i>, a stable LMM isolated from an EMS-induced libraryof wheat cultivar AK58. <i>lm10373</i> developed light-dependent lesion spots on leavesfrom the late tillering stage, accompanied by programmed cell death (PCD) andreactive oxygen species (ROS) accumulation. Phenotypically, <i>lm10373</i> showedreduced photosynthetic capacity and yield-related traits, but enhanced powdery mildewresistance at the heading stage. Genetic analysis revealed the lesion trait wascontrolled by a single semi-dominant nuclear gene, mapped to a 35 Mb interval onchromosome 3B via bulked segregant analysis coupled with exome capturesequencing (BSE-seq). Integrating exome sequencing and transcriptome data, weidentified <i>TaWSD1-3B</i> (encoding an O-acyltransferase of the WSD1 family) as thecausal gene. A G-to-A mutation (p.Ala79Thr) in its conserved acyltransferase domainintroduced a new phosphorylation site, disrupting triacylglycerol biosynthesis. Twoindependent mutants (<i>lm129</i>, p.Arg207His; <i>lm295</i>, 3'UTR mutation) validatedTaWSD1-3B function. Haplotype analysis of 183 wheat accessions identified three<i>TaWSD1-3B</i> haplotypes: <i>Hap1</i> was associated with higher 1000-grain weight andlower leaf tip necrosis (LTN) severity, making it a favorable allele for breeding. Thisstudy characterized a wheat LMM mutant and candidate gene <i>TaWSD1-3B</i>,suggesting a lipid-ROS-PCD pathway regulating immunity, and provides valuablemarkers for stress-tolerant, high-yield wheat breeding.</p>

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Characterization, genetic analysis and gene identification of an EMS-mutagenized lesion-mimic mutant with enhanced powdery mildew resistance in bread wheat (Triticum aestivum L.)

  • 期刊论文

  • 发表日期：

    2026年3月4日

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  • Yanzhen Hu,
  • Pan Liu,
  • Lifeng Du,
  • Dengke Wang,
  • Guangyao Zhao,
  • Zhaofeng Li,
  • Xiangzheng Liao,
  • Zefu Lu,
  • Jizeng Jia,
  • Lifeng Gao

摘要

Lesion mimic mutants (LMMs) are ideal for dissecting plant immunity mechanisms.Here, we characterized lm10373, a stable LMM isolated from an EMS-induced libraryof wheat cultivar AK58. lm10373 developed light-dependent lesion spots on leavesfrom the late tillering stage, accompanied by programmed cell death (PCD) andreactive oxygen species (ROS) accumulation. Phenotypically, lm10373 showedreduced photosynthetic capacity and yield-related traits, but enhanced powdery mildewresistance at the heading stage. Genetic analysis revealed the lesion trait wascontrolled by a single semi-dominant nuclear gene, mapped to a 35 Mb interval onchromosome 3B via bulked segregant analysis coupled with exome capturesequencing (BSE-seq). Integrating exome sequencing and transcriptome data, weidentified TaWSD1-3B (encoding an O-acyltransferase of the WSD1 family) as thecausal gene. A G-to-A mutation (p.Ala79Thr) in its conserved acyltransferase domainintroduced a new phosphorylation site, disrupting triacylglycerol biosynthesis. Twoindependent mutants (lm129, p.Arg207His; lm295, 3'UTR mutation) validatedTaWSD1-3B function. Haplotype analysis of 183 wheat accessions identified threeTaWSD1-3B haplotypes: Hap1 was associated with higher 1000-grain weight andlower leaf tip necrosis (LTN) severity, making it a favorable allele for breeding. Thisstudy characterized a wheat LMM mutant and candidate gene TaWSD1-3B,suggesting a lipid-ROS-PCD pathway regulating immunity, and provides valuablemarkers for stress-tolerant, high-yield wheat breeding.