{'fraction_non_alphanumeric': 0.02375, 'fraction_numerical': 0.008125, 'mean_word_length': 5.8418803418803416, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Mechanistic dissection of accelerated cell death and multiple disease resistance in a maize lethal leaf spot 1 allele.

Multiple disease resistance (MDR) has attracted increasing attention in maize. However, the interplay between cell death and metabolite changes and their contributions to MDR remains elusive in maize. In this study, we identified a disease lesion mimic 30 (les30) mutant that showed suicidal lesion formation and enhanced resistance to Curvularia lunata (Wakker) Boed. By map-based cloning, a gene encoding the pheophorbide a oxidase (PAO/LLS1) known to be involved in chlorophyll degradation and MDR was found to be the causal gene. LLS1 was found induced by both biotic and abiotic stresses. Based on transcriptomics analysis, genes involved in defense response and secondary metabolite biosynthesis were mildly activated in les30 leaves without lesion, while those processes were dramatically amplified in lesioned les30 leaves. Moreover, the defense-associated phytohormones including jasmonic acid and salicylic acid, and phytoalexins including phenylpropanoids, lignin and flavonoids were over-accumulated in the lesioned les30 leaves, suggesting the activation of defense-associated phytohormone and metabolite biosynthesis in a lesion-dependent manner. In general, this study implies the existence of an interactive amplification loop of interrupted chlorophyll degradation, cell death, defense-related gene expressions, and metabolite changes resulting in suicidal lesion formation and MDR, which allows potential genetic manipulation to improve maize disease resistance.