Phytochrome B enhances seed germination tolerance to high temperature by reducing S-nitrosylation of HFR1.

Abstract

Light and ambient high temperature (HT) have opposite effects on seed germination. Light induces seed germination through activating the photoreceptor phytochrome B (phyB), resulting in the stabilization of the transcription factor HFR1, which in turn sequesters the suppressor PIF1. HT suppresses seed germination and triggers protein S-nitrosylation. Here, we find that HT suppresses seed germination by inducing the S-nitrosylation of HFR1 at C164, resulting in its degradation, the release of PIF1, and the activation of PIF1-targeted SOMNUS (SOM) expression to alter gibberellin (GA) and abscisic acid (ABA) metabolism. Active phyB (phyBY276H ) antagonizes HFR1 S-nitrosylation and degradation by increasing S-nitrosoglutathione reductase (GSNOR) activity. In line with this, substituting cysteine-164 of HFR1 with serine (HFR1C164S ) abolishes the S-nitrosylation of HFR1 and decreases the HT-induced degradation of HFR1. Taken together, our study suggests that HT and phyB antagonistically modulate the S-nitrosylation level of HFR1 to coordinate seed germination, and provides the possibility to enhance seed thermotolerance through gene-editing of HFR1.