RcSRR1 interferes with the RcCSN5B-mediated deneddylation of RcCRL4 to modulate RcCO proteolysis and prevent rose flowering under red light.

Light is essential for rose (Rosa spp.) growth and development. Different light qualities play differing roles in the rose floral transition, but the molecular mechanisms underlying their effects are not fully understood. Here, we observed that red light suppresses rose flowering and increases the expression of sensitivity to red light reduced 1 (RcSRR1) compared with white light. Virus-induced gene silencing (VIGS) of RcSRR1 led to early flowering under white light and especially under red light, suggesting that this gene is a flowering repressor with a predominant function under red light. We determined that RcSRR1 interacts with the COP9 signalosome subunit 5B (RcCSN5B), while RcCSN5B, RcCOP1, and RcCO physically interact with each other. Furthermore, the RcCSN5B-induced deneddylation of Cullin4-RING E3 ubiquitin ligase (RcCRL4) in rose was reduced by the addition of RcSRR1, suggesting that the interaction between RcSRR1 and RcCSN5B relieves the deneddylation of the RcCRL4-COP1/SPA complex to enhance RcCO proteolysis, which subsequently suppresses the transcriptional activation of RcFT and ultimately flowering. Far-red light-related sequence like 1 (RcFRSL3) was shown to specifically bind to the G-box motif of the RcSRR1 promoter to repress its transcription, removing its inhibition of RcFT expression and inducing flowering. Red light inhibited RcFRSL3 expression, thereby promoting the expression of RcSRR1 to inhibit flowering. Taken together, these results provide a previously uncharacterized mechanism by which the RcFRSL3-RcSRR1-RcCSN5B module targets RcCO stability to regulate flowering under different light conditions in rose plants.