Nitric oxide promotes light-initiated seed germination by repressing PIF1 expression and stabilizing HFR1.

Seed germination is a crucial stage in the life cycle of plants and is tightly controlled by internal and external signals. Phytochrome photoreceptors perceive light stimulation to promote seed germination. Previous studies have shown that PHYTOCHROME-INTERACTION FACTOR 1 (PIF1) is a negative regulatory factor and represses seed germination, while LONG HYPOCOTYL IN FAR-RED (HFR1) sequesters PIF1 by forming a heterodimer to relieve the inhibitory effect of seed germination during the initial phase. Nitric oxide (NO) has been reported to break seed dormancy, but the underlying mechanism is not well understood. Here, we report that NO signal enhances phytochrome B (PHYB)-dependent seed germination, and PHYB perceives red light stimulation to activate NR activity and NO accumulation. NO signal not only downregulates the transcription of PIF1, but also stabilize HFR1 proteins to intensify the interaction of the HFR1-PIF1 heterodimer, and compensate for the inhibitory effect of PIF1 on its target genes associated with hormone metabolism and cell wall loosening, consequently initiating seed germination. Thus, our results reveal a new mechanism for NO signals in modulating PHYB-mediated seed germination by repressing PIF1 expression at the transcriptional level as well as preventing PIF1 activity by stabilizing HFR1 protein.

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