THF_1 mutations lead to increased basal and wound-induced levels of oxylipins that stimulate anthocyanin biosynthesis via COI_1 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（COM）signaling.Our data showed that thf1 had higher levels of basalα-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.

Defective Etioplasts Observed in Variegation Mutants May Reveal the Light-Independent Regulation of White/Yellow Sectors of Arabidopsis Leaves

Leaf variegation resulting from nuclear gene mutations has been used as a model system to elucidate the molecular mechanisms of chloroplast development. Since most variegation genes also function in photosynthesis, it remains unknown whether their roles in photosynthesis and chloroplast development are distinct. Here, using the variegation mutant thylakoid formation1 （thfl） we show that variegation formation is light independent. It was found that slow and uneven chloroplast development in thfl can be attributed to defects in etioplast development in darkness. Ultrastructural analysis showed the coexistence of plastids with or without prolamellar bodies （PLB） in cells of thfl, but not of WT. Although THF1 mutation leads to significant decreases in the levels of Pchlide and Pchliide oxidoreductase （POR） expression, genetic and 5-aminolevulinic acid （ALA）-feeding analysis did not reveal Pchlide or POR to be critical factors for etioplast formation in thfl. Northern blot analysis showed that plastid gene expression is dramatically reduced in thfl compared with that in WT, particularly in the dark. Our results also indicate that chlorophyll biosynthesis and expression of plastidic genes are coordinately suppressed in thfl. Based on these results, we propose a model to explain leaf variegation formation from the plastid development perspective.