Circadian Clock Proteins LHY and CCA1 Regulate SVP Protein Accumulation to Control Flowering in Arabidopsis
Author(s) -
Sumire Fujiwara,
Atsushi Oda,
Riichiro Yoshida,
Kanae Niinuma,
Kana Miyata,
Yusuke Tomozoe,
Takeomi Tajima,
Mayu Nakagawa,
Kounosuke Hayashi,
George Coupland,
Tsuyoshi Mizoguchi
Publication year - 2008
Publication title -
the plant cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.324
H-Index - 341
eISSN - 1532-298X
pISSN - 1040-4651
DOI - 10.1105/tpc.108.061531
Subject(s) - biology , circadian clock , arabidopsis , photoperiodism , gigantea , genetics , mutant , repressor , flowering locus c , mads box , transcription factor , vernalization , locus (genetics) , botany , microbiology and biotechnology , gene
The floral regulators GIGANTEA (GI), CONSTANS (CO), and FLOWERING LOCUS T (FT) play key roles in the photoperiodic flowering responses of the long-day plant Arabidopsis thaliana. The GI-CO-FT pathway is highly conserved in plants. Here, we demonstrate that the circadian clock proteins LATE ELONGATED HYPOCOTYL (LHY) and CIRCADIAN CLOCK-ASSOCIATED1 (CCA1) not only repressed the floral transition under short-day and long-day conditions but also accelerated flowering when the plants were grown under continuous light (LL). LHY and CCA1 accelerated flowering in LL by promoting FT expression through a genetic pathway that appears to be independent of the canonical photoperiodic pathway involving GI and CO proteins. A genetic screen revealed that the late-flowering phenotype of the lhy;cca1 double mutant under LL was suppressed through mutations in SHORT VEGETATIVE PHASE (SVP), a MADS box transcription factor. Yeast two-hybrid analysis demonstrated an interaction between SVP and FLOWERING LOCUS C, and genetic analysis indicated that these two proteins act as partially redundant repressors of flowering time. SVP protein accumulated in lhy;cca1 plants under LL. We propose a model in which LHY and CCA1 accelerate flowering in part by reducing the abundance of SVP and thereby antagonizing its capacity to repress FT expression under LL.
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