THF1 mutations lead to increased basal and wound-induced levels of oxylipins that stimulate anthocyanin biosynthesis via COI1 signaling in Arabidopsis.

摘要: Mutants defective in chloroplast development or photosynthesis are liable to accumulate higher levels of anthocyanin photo-oxidative stress. However, regulatory mechanisms biosynthesis the mutants remain unclear. Here, we investigated mechanism by which deletion thylakoid formation1 (THF1) leads an increased level Arabidopsis thaliana L. Physiological and genetic evidence showed that thf1 is dependent on coronatine-insensitive1 (COI1) signaling. Our data had basal α-linolenic acid (α-LeA), methyl jasmonate (JA)-induced α-LeA 12-oxophytodienoic (OPDA) than wild type (WT). Consistently, expression phospholipase genes including pPLAIIα PLA-Iγ1 were elevated thf1. Furthermore, inhibition lipase activity bromoenol lactone, a specific inhibitor plant pPLA, led producing identical anthocyanins WT plants. Interestingly, OPDA was triggered light illumination isolated chloroplasts, indicating new protein import into chloroplasts not required for biosynthesis. Thus, conclude accumulation attributed increase JA levels. This JA-mediated signaling coordinate metabolism growth stress may be conserved other photosensitive mutants.