Molecular Basis Of Jasmonate-induced Anthocyanin Accumulation And Leaf Senescence In Arabidopsis

Jasmonates (JAs), which are synthesized from the octadecanoid/ hexadecanoid pathways, control many plant developmental and growth processes, and mediate plant responses to abiotic and biotic stresses. The F-box protein coronatine insensitive 1 (COI1) is a key regulator in JA signal pathway. It directly binds to JA-Ile and functions as a JA receptor. COI1 interacts with AtCUL1, AtRbx1, and either of the Arabidopsis Skp1-like proteins ASK1 or ASK2 to assemble the SCFCOI1 complex, which recruits jasmonate ZIM-domain proteins (JAZs) for degradation by the 26S proteasome and subsequently regulates expression of various genes. The null mutant coi1-1, with the premature stop codon at W467, is male sterile, insensitive to JA-inhibitory root growth, defective in JA-regulated gene expression, and super-sensitive to insect attack and pathogen infection.JA has been shown to induce anthocyanin accumulation in several plant species, however, the molecular mechanism for JA-regulated anthocyanin accumulation remains unknown. In this study, physiological and molecular evidence is presented to reveal that (i) JA-induced anthocyanin accumulation is primarily via up-regulation of the'late'anthocyanin biosynthetic genes DFR, LDOX, and UF3GT, and COI1 is essential for the JA-induced expression of these anthocyanin biosynthetic'late'genes. (ii) The expression of anthocyanin biosynthetic regulators, PAP1, PAP2, and GL3 is significantly induced by JA, and COI1 is required for JA-induced PAP1, PAP2, and GL3 transcription. Thus, it is speculated that COI1 regulates the expression of the transcription factors, including PAP1, PAP2, and GL3, which mediates the'late'anthocyanin biosynthetic genes DFR, LDOX, and UF3GT, and thereby modulates JA-induced anthocyanin biosynthesis in Arabidopsis. (iii) Mutation in COI1 is unable to abolish the cytokinin- and sugar-induced anthocyanin biosynthesis. (iv) Sugar is required for specific induction of anthocyanin biosynthesis by JA and cytokinin.JA is also found to play an important role in leaf senescence. In Arabidopsis, exogenous application of JA promotes leaf senescence and regulates expression of various genes which are involved in leaf senescence. The coi1 mutant plants also exhibit delayed senescence phenotypes including elongated flowering time and relatively higher chlorophyll content. However, the molecular mechanism for JA and COI1 function in leaf senescence is not clear. In this study, proteomic, genetic, and physiological approaches are used to reveal the molecular basis of JA-regulated leaf senescence in Arabidopsis. We identified 35 COI1-dependent JA-regulated proteins using two-dimensional fluorescenc differential gel electrophoresis in Arabidopsis. Among these 35 proteins, ribulose bisphosphate carboxylase oxygenase activase (RCA) was a COI1-dependent JA-repressed protein. We found that RCA was down-regulated at the levels of transcript and protein abundance by JA in COI1 dependent manner. We further demonstrated that loss of RCA caused leaf senescence and that JA-induced leaf senescence resulted from the COI1-dependent JA-repressed RCA expression. In addition, the T-DNA insertional mutation in RCA led to a decrease in JA-inducible expression of COR1, PDF1.2 and Thi2.1, implying a role for RCA in JA-regulated plant defense.