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

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

KEYWORDS: {{ getKeywords(articleDetailText.words) }}