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AtBBX21 and COP1 genetically interact in the regulation of shade avoidance

Colaborador(es): Crocco, Carlos Daniel | Holm, M | Yanovsky, Marcelo J | Botto, Javier Francisco.
ISSN: 1365-313X.Tipo de material: Artículos y capítulos. Recurso electrónico.Tema(s): ARABIDOPSIS | B-BOX ZINC FINGER PROTEINS | CANOPY LIGHT | PAR GENES | SHADE-AVOIDANCE SYNDROME | T-DNA MUTANTS | GENES | SEED | TRANSCRIPTION FACTORS | ZINC | TRANSCRIPTION | ARABIDOPSIS PROTEIN | BASIC HELIX LOOP HELIX TRANSCRIPTION FACTOR | BBX21 PROTEIN, ARABIDOPSIS | COP1 PROTEIN, ARABIDOPSIS | PAR1 PROTEIN, ARABIDOPSIS | TRANSCRIPTION FACTOR | UBIQUITIN PROTEIN LIGASE | GENE EXPRESSION PROFILING | GENE EXPRESSION REGULATION | GENETICS | GROWTH, DEVELOPMENT AND AGING | METABOLISM | MUTATION | PHOTOTROPISM | PLANT GENE | SUNLIGHT | UPREGULATION | ARABIDOPSIS PROTEINS | BASIC HELIX-LOOP-HELIX TRANSCRIPTION FACTORS | GENE EXPRESSION REGULATION, PLANT | GENES, PLANT | UBIQUITIN-PROTEIN LIGASES | UP-REGULATION | Recursos en línea: Haga clic para acceso en línea | LINK AL EDITOR. En: The Plant Journal vol.64, no.4 (2010), p.551-562Resumen: Plants grown at high densities perceive the reduction in the ratio of red [R] to far-red [FR] light as a warning of competition. This light signal triggers morphological responses such as hypocotyl and stem elongation, and acceleration of flowering, which are known collectively as the shade-avoidance syndrome [SAS]. Mutations in the photomorphogenic repressor COP1 suppress the SAS, but how COP1 modulates these responses is uncertain. We identified a new mutant with altered responses to natural shade, named lhus [long hypocotyl under shade]. lhus seedlings have longer hypocotyls than wild-type under a low R:FR ratio, but not under sunlight or darkness. The lhus phenotype is due to a mutation affecting a B-box zinc finger transcription factor encoded by At1g75540, a gene previously reported as AtBBX21 that interacts with COP1 to control de-etiolation. Mutations in genes encoding other members of this protein family also result in impaired SAS regulation. Under short-term canopy shade, LHUS/BBX21 acts as positive regulator of SAS genes such as PAR1, HFR1, PIL1 and ATHB2. In contrast, global expression analysis of wild-type and lhus/bbx21 seedlings revealed that a large number of genes involved in hormonal signalling pathways are negatively regulated by LHUS/BBX21 in response to long-term canopy shade, and this observation fits well with the phenotype of lhus/bbx21 seedlings grown under a low R:FR ratio. Moreover, the bbx21 bbx22 double mutation restored the SAS in the cop1 background. We propose that LHUS/BBX21 and other B-box-containing proteins, such as BBX22, act downstream of COP1, and play a central role in early and long-term adjustment of the SAS in natural environments.
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Plants grown at high densities perceive the reduction in the ratio of red [R] to far-red [FR] light as a warning of competition. This light signal triggers morphological responses such as hypocotyl and stem elongation, and acceleration of flowering, which are known collectively as the shade-avoidance syndrome [SAS]. Mutations in the photomorphogenic repressor COP1 suppress the SAS, but how COP1 modulates these responses is uncertain. We identified a new mutant with altered responses to natural shade, named lhus [long hypocotyl under shade]. lhus seedlings have longer hypocotyls than wild-type under a low R:FR ratio, but not under sunlight or darkness. The lhus phenotype is due to a mutation affecting a B-box zinc finger transcription factor encoded by At1g75540, a gene previously reported as AtBBX21 that interacts with COP1 to control de-etiolation. Mutations in genes encoding other members of this protein family also result in impaired SAS regulation. Under short-term canopy shade, LHUS/BBX21 acts as positive regulator of SAS genes such as PAR1, HFR1, PIL1 and ATHB2. In contrast, global expression analysis of wild-type and lhus/bbx21 seedlings revealed that a large number of genes involved in hormonal signalling pathways are negatively regulated by LHUS/BBX21 in response to long-term canopy shade, and this observation fits well with the phenotype of lhus/bbx21 seedlings grown under a low R:FR ratio. Moreover, the bbx21 bbx22 double mutation restored the SAS in the cop1 background. We propose that LHUS/BBX21 and other B-box-containing proteins, such as BBX22, act downstream of COP1, and play a central role in early and long-term adjustment of the SAS in natural environments.

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