MYC2, MYC3, and MYC4 function additively in wounding-induced jasmonic acid biosynthesis and catabolism.

Abstract

Jasmonic acid (JA) plays a critical role in plant defenses against insects and necrotrophic fungi. Wounding or lepidopteran insect feeding rapidly induces a burst of JA in plants, which usually reaches peak values within 1 to 2 h. The induced JA is converted to JA-Ile and perceived by the COI1-JAZ co-receptor, leading to activation of the transcription factors MYC2 and its homologs, which further induce JA-responsive genes. Although much is known about JA biosynthesis and catabolism enzymes and JA signaling, how JA biosynthesis and catabolism are regulated remain unclear. Here, we show that in Arabidopsis thaliana MYC2 functions additively with MYC3 and MYC4 to regulate wounding-induced JA accumulation by directly binding to the promoters of genes function in JA biosynthesis and catabolism to promote their transcription. MYC2 also controls the transcription of JAV1 and JAM1, which are key factors controlling JA biosynthesis and catabolism, respectively. In addition, we also found that MYC2 could bind to the MYC2 promoter and self-inhibit its own expression. This work illustrates the central role of MYC2/3/4 in controlling wounding-induced JA accumulation by regulating the transcription of genes involved in JA biosynthesis and catabolism.