AtBBX21 and COP1 genetically interact in the regulation of shade avoidance

CARLOS D. CROCCO, MAGNUS HOLM, MARCELO J. YANOVSKY, JAVIER F. BOTTO

PLANT JOURNAL

WILEY-BLACKWELL PUBLISHING, INC

Año: 2010 vol. 64 p. 551 - 565

0960-7412

Plants grown at high densities perceive, through the phytochrome system, the selective absorption of red (R) by canopy leaves, and reflection of far-red (FR) from neighbour plants. This signal triggers morphological responses such as hypocotyl, stem and petiole elongation, and acceleration of flowering, which are known collectively as the shade-avoidance syndrome (SAS). Mutations in the photomorphogenic repressor COP1 suppress SAS, but how COP1 modulates these responses is uncertain. We identified a new mutant with altered responses to natural shade, named lhus for long hypocotyl under shade. lhus seedlings have longer hypocotyls than wild-type under low R:FR, but not under sunlight or darkness. 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 other members of this protein family are also impaired in SAS regulation. In 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 reveals that a large number of genes involved in hormonal signalling pathways are negatively regulated by LHUS/BBX21 in response to a long-term canopy shade, and this observation fits well with the phenotype of lhus/bbx21 seedlings grown under low R:FR. Moreover, bbx21bbx22 restored SAS in the cop1 background. We propose that LHUS/BBX21 and other B-box-containing proteins, such as BBX22, act downstream of COP1 playing a central function in the early and long-term adjustment of SAS in natural environments.