SmbHLH37 Functions Antagonistically With SmMYC2 in Regulating Jasmonate-Mediated Biosynthesis of Phenolic Acids in Salvia miltiorrhiza

Abstract

Jasmonates (JAs) are integral to various defense responses and induce biosynthesis of many secondary metabolites. MYC2, a basic helix-loop-helix (bHLH) transcription factor (TF), acts as a transcriptional activator of JA signaling. MYC2 is repressed by the JASMONATE ZIM-domain (JAZ) proteins in the absence of JA, but de-repressed by the protein complex SCF^COI1 on perception of JA. We previously reported that overexpression of <i>SmMYC2</i> promotes the production of salvianolic acid B (Sal B) in <i>Salvia miltiorrhiza.</i> However, the responsible molecular mechanism is unclear. Here, we showed that SmMYC2 binds to and activates the promoters of its target genes <i>SmTAT1</i>, <i>SmPAL1</i>, and <i>SmCYP98A14</i> to activate Sal B accumulations. <i>SmbHLH37</i>, a novel bHLH gene significantly up-regulated by constitutive expression of <i>SmMYC2</i>, was isolated from <i>S. miltiorrhiza</i> for detailed functional characterization. SmbHLH37 forms a homodimer and interacts with SmJAZ3/8. Overexpression of <i>SmbHLH37</i> substantially decreased yields of Sal B. SmbHLH37 binds to the promoters of its target genes <i>SmTAT1</i> and <i>SmPAL1</i> and blocks their expression to suppress the pathway for Sal B biosynthesis. These results indicate that SmbHLH37 negatively regulates JA signaling and functions antagonistically with SmMYC2 in regulating Sal B biosynthesis in <i>S. miltiorrhiza</i>.