phyB Interacts with BES1 to Regulate Brassinosteroid Signaling in Arabidopsis.

Light is an important environmental factor, which mainly inhibits hypocotyl elongation through various photoreceptors. In contrast, brassinosteroids (BR) are major hypocotyl elongation-promoting hormones in plants, which could optimize photomorphogenesis in concurrent with external light. However, the precise molecular mechanisms underlying the antagonism of light and BR signaling remain largely unknown. Here we show that Arabidopsis red light receptor phyB involves in inhibition of BR signaling via its direct interaction with BR transcription factor BES1. In our study, phyB mutant displays BR hypersensitivity, which is repressed in transgenic plants overexpressing phyB, suggests that phyB negatively regulates BR signaling pathway. In addition, protein interaction results show that phyB directly interacts with dephosphorylated BES1, the physiologically active form of BES1 induced by BR, in a red light-dependent manner. Genetic analyses suggest that phyB may act partially through BES1 to regulate BR signaling. Transcriptomic data and qRT-PCR assay further show that phyB-mediated red light inhibits BR signaling by repressing BES1 target genes expression, including the BR biosynthesis genes DWF4, the SAUR family and the PRE family genes required for promoting cell elongation. Finally, we found red light treatment inhibits the DNA-binding activity of BES1 and photoactivated phyB represses the transcriptional activity of BES1 under red light. Taken together, we suggest that the interaction of phyB with dephosphorylated BES1 may allow plants to balance light and BR signaling by repressing transcriptional activity of BES1 to regulate its target genes expression.