The cyclophilin ROC1 links phytochrome and cryptochrome to brassinosteroid sensitivity.

Although multiple photoreceptors converge to control common aspects of seedling de-etiolation, we are relatively ignorant of the genes acting at or downstream of their signalling convergence. To address this issue we screened for mutants under a mixture of blue plus far-red light and identified roc1-1D. The roc1-1D mutant, showing elevated expression of the ROTAMASE CYCLOPHILIN 1 (ROC1/AtCYP18-3) gene, and partial loss-of function roc1 alleles, has defects in phytochrome A (phyA)-, cryptochrome 1 (cry1)- and phytochrome B (phyB)-mediated de-etiolation, including long hypocotyls under blue or far-red light. These mutants show elevated sensitivity to brassinosteroids in the light but not in the dark. Mutations at brassinosteroid signalling genes and the application of a brassinosteroid synthesis inhibitor eliminated the roc1 and roc1-D phenotypes. The roc1 and roc1-D mutants show altered patterns of phosphorylation of the transcription factor BES1, a known point of control of sensitivity to brassinosteroids, which correlate with the expression levels of genes directly targeted by BES1. We propose a model where perception of light by phyA, cry1 or phyB activates ROC1 (at least in part by enhancing its expression). This in turn reduces the intensity of brassinosteroid signalling and fine-tunes seedling de-etiolation.

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