S-nitrosylation of the transcription factor MYB30 facilitates nitric oxide-promoted seed germination in Arabidopsis.

Abstract

The gaseous signaling molecule nitric oxide (NO) plays an important role in breaking seed dormancy. NO induces a decrease in abscisic acid (ABA) content by transcriptionally activating its catabolic enzyme, the ABA 8'-hydroxylase CYP707A2. However, the underlying mechanism of this process remains unclear. Here, we report that the transcription factor MYB30 plays a critical role in NO-induced seed germination in Arabidopsis (Arabidopsis thaliana). MYB30 loss-of-function attenuates NO-mediated seed dormancy breaking. MYB30 triggers a NO-induced decrease in ABA content during germination by directly promoting CYP707A2 expression. NO induces S-nitrosylation at Cys-49 of MYB30 and enhances its transcriptional activity. Conversely, the ABA receptors PYRABACTIN RESISTANCE1 (PYR1)/PYR1-LIKE (PYL)/REGULATORY COMPONENTS OF ABA RECEPTORS (RCAR) interact with MYB30 and repress its transcriptional activity. ABA promotes the interaction between PYL4 and MYB30, whereas S-nitrosylation releases the PYL4-mediated inhibition of MYB30 by interfering with the PYL4-MYB30 interaction. Genetic analysis showed that MYB30 functions downstream of PYLs during seed dormancy and germination in response to NO. Furthermore, MYB30 mutation significantly represses the reduced dormancy phenotype and the enhanced CYP707A2 expression of the pyr1 pyl1 pyl2 pyl4 quadruple mutant. Our findings reveal that S-nitrosylation of MYB30 precisely regulates the balance of seed dormancy and germination, providing insights into the underlying mechanism of NO-promoted seed germination.