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 (phyB Y276H) antagonizes HFR1 S‐nitrosylation and degradation by increasing S‐nitrosoglutathione reductase (GSNOR) activity. In line with this, substituting cysteine‐164 of HFR1 with serine (HFR1 C164S) 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.