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...
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| Otros Autores: | , |
| Formato: | Artículo |
| Lenguaje: | Inglés |
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| Acceso en línea: | http://ri.agro.uba.ar/files/intranet/articulo/2012Trupkin.pdf LINK AL EDITOR |
| Aporte de: | Registro referencial: Solicitar el recurso aquí |
| Sumario: | 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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| ISSN: | 1365-313X (en línea) 0960-7412 (impreso) |