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The cyclophilin ROC1 links phytochrome and cryptochrome to brassinosteroid sensitivity

Por: Trupkin, Santiago A.
Colaborador(es): Mora García, Santiago | Casal, Jorge José.
ISSN: 1365-313X.Tipo de material: Artículos y capítulos. Recurso electrónico.Tema(s): ARABIDOPSIS | BRASSINOSTEROID | CRYPTOCHROME | PHYTOCHROME | ROTAMASE CYCLOPHILIN 1 | BRASSINOSTEROIDS | CRYPTOCHROMES | CYCLOPHILIN | PHOSPHORYLATION | PLANTS [BOTANY] | TRANSCRIPTION FACTORS | GENES | ARABIDOPSIS PROTEIN | BES1 PROTEIN, ARABIDOPSIS | CRY1 PROTEIN, ARABIDOPSIS | NUCLEAR PROTEIN | PHYTOCHROME A | ROC1 PROTEIN, ARABIDOPSIS | GENETICS | LIGHT | METABOLISM | MUTATION | PHENOTYPE | PHOSPHORYLATION | ARABIDOPSIS PROTEINS | BRASSINOSTEROIDS | NUCLEAR PROTEINS | PHYTOCHROME A | Recursos en línea: Haga clic para acceso en línea | LINK AL EDITOR. En: The Plant Journal vol.71, no.5 (2012), p.712-723Resumen: 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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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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