Transcriptomic and metabolomic analyses reveal OsACL-A2 coordinates light signaling, stress responses, and metabolic...

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.

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.

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).

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.