DnaJ proteins, also known as HSP40s, play a key role in plant growth and development, and response to environmental stress. However, little comprehensive research has been conducted on the DnaJ gene family in maize. Here, we identify 91 ZmDnaJ genes from maize, which are likely distributed in the chloroplast, nucleus, and cytoplasm. Our analysis revealed that ZmDnaJs were classified into three types, with conserved protein motifs and gene structures within the same type, particularly among members of the same subfamily. Gene duplication events have likely contributed to the expansion of the ZmDnaJ family in maize. Analysis of cis-regulatory elements in ZmDnaJ promoters suggested involvement in stress responses, growth and development, and phytohormone sensitivity in maize. Specifically, four cis-acting regulatory elements associated with stress responses and phytohormone regulation indicated a role in adaptation. RNA-seq analysis showed constitutive expression of most ZmDnaJ genes, some specifically in pollen and endosperm. More importantly, certain genes also responded to salt, heat, and cold stresses, indicating potential interaction between stress regulatory networks. Furthermore, early responses to heat stress varied among five inbred lines, with upregulation of almost tested ZmDnaJ genes in B73 and B104 after 6 h, and fewer genes upregulated in QB1314, MD108, and Zheng58. After 72 h, most ZmDnaJ genes in the heat-sensitive inbred lines (B73 and B104) returned to normal levels, while many genes, including ZmDnaJ55, 79, 88, 90, and 91, remained upregulated in the heat-tolerant inbred lines (QB1314, MD108, and Zheng58) suggesting a synergistic function for prolonged protection against heat stress. In conclusion, our study provides a comprehensive analysis of the ZmDnaJ family in maize and demonstrates a correlation between heat stress tolerance and the regulation of gene expression within this family. These offer a theoretical basis for future functional validation of these genes.

Introduction: Lesion mimic mutants (LMMs) spontaneously develop defense-related cell death lesions, serving as ideal models for studying plant immunity. However, the metabolic mechanisms underlying light-dependent lesion formation remain poorly understood. Methods: To address this, we performed comparative transcriptomic and metabolomic analyses on wild-type rice and the lmm64 mutant, which carries a novel allele of OsACL-A2 , under light and dark conditions. Results: The lmm64 mutant develops light-dependent lesions accompanied by ROS accumulation. Transcriptomic analysis revealed 750 lesion-associated genes specifically altered under light, which were enriched in stress responses, light signaling, carbon metabolism, and secondary metabolism. Stress-responsive genes were predominantly upregulated. Multiple light signaling components (e.g., HY5 , PIF3 ) showed marked transcriptional changes. Meanwhile, acetyl-CoA metabolism-related genes ( ACS , PDHA1 , ACO ) were upregulated, likely as a compensatory response to OsACL-A2 dysfunction, while glycolytic genes ( PFK1 , PK , ADH ) were downregulated. At the metabolic level, phenolic compounds including flavonoids and phenolic acids were significantly reduced, consistent with the downregulation of key phenylpropanoid/flavonoid biosynthetic genes (e.g., CHS , CHI , F3'H , 4CL2 , HCT ). Conclusion: These findings reveal that OsACL-A2 integrates light signaling, stress responses, and metabolic reprogramming to orchestrate light-dependent lesion formation in rice, expanding its known functions.