Programmed cell death (PCD) is an important form to protect plants from pathogen attack. However, plants must precisely control the PCD process under microbe attacks to avoid detrimental effects. The complexity of how plants balance the defense activation and PCD requires further clarification. Lesion mimic mutants constitute an excellent material to study the crosstalk between them. Here, we identified a (cotton) lesion mimic mutant (), which exhibits necrotic leaf damage and enhanced disease resistance. Map-based cloning demonstrated that , encoding 5-aminolevulinic acid dehydratase and located on chromosome D5, was responsible for the phenotype. The mutant was resulted from a nonsense mutation within the coding region of It exhibited an overaccumulation of the 5-aminolevulinic acid, elevated levels of reactive oxygen species and salicylic acid, along with constitutive expression of pathogenesis-related genes and enhanced resistance to the infection. Interestingly, plays a dosage-dependent role in regulating PCD of cotton leaves and resistance to infection. This study provides a new strategy on the modulation of plant immunity, particularly in polyploidy plants.

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HighlightTransgenic evidence is provided that the expression of a cotton endo-1,4-β-glucanase, GhKOR1, is required for endosperm cellularization, cotton fibre cellulose synthesis, and the establishment of seedling vigour

Summary Anthocyanin accumulations in the flowers can improve seed production of hybrid lines, and produce higher commodity value in cotton fibre. However, the genetic mechanism underlying the anthocyanin pigmentation in cotton petals is poorly understood. Here, we showed that the red petal phenotype was introgressed from Gossypium bickii through recombination with the segment containing the R3 bic region in the A07 chromosome of Gossypium hirsutum variety LR compared with the near‐isogenic line of LW with white flower petals. The cyanidin‐3‐O‐glucoside (Cy3G) was the major anthocyanin in red petals of cotton. A GhTT19 encoding a TT19‐like GST was mapped to the R3bic site associated with red petals via map‐based cloning, but GhTT19 homologue gene from the D genome was not expressed in G. hirsutum. Intriguingly, allelic variations in the promoters between GhTT19LW and GhTT19LR, rather than genic regions, were found as genetic causal of petal colour variations. GhTT19‐GFP was found localized in both the endoplasmic reticulum and tonoplast for facilitating anthocyanin transport. An additional MYB binding element found only in the promoter of GhTT19LR, but not in that of GhTT19LW, enhanced its transactivation by the MYB activator GhPAP1. The transgenic analysis confirmed the function of GhTT19 in regulating the red flower phenotype in cotton. The essential light signalling component GhHY5 bonded to and activated the promoter of GhPAP1, and the GhHY5‐GhPAP1 module together regulated GhTT19 expression to mediate the light‐activation of petal anthocyanin pigmentation in cotton. This study provides new insights into the molecular mechanisms for anthocyanin accumulation and may lay a foundation for faster genetic improvement of cotton.