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High‐level expression and phosphorylation of phytochrome B modulates flowering time in Arabidopsis
Author(s) -
Hajdu Anita,
Ádám Éva,
Sheerin David J.,
Dobos Orsolya,
Bernula Péter,
Hiltbrunner Andreas,
KozmaBognár László,
Nagy Ferenc
Publication year - 2015
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12926
Subject(s) - phytochrome , arabidopsis , biology , circadian clock , photoperiodism , ubiquitin ligase , microbiology and biotechnology , gigantea , transcription factor , mutant , cryptochrome , phytochrome a , genetics , gene , ubiquitin , botany , red light
Summary Optimal timing of flowering in higher plants is crucial for successful reproduction and is coordinated by external and internal factors, including light and the circadian clock. In Arabidopsis, light‐dependent stabilization of the rhythmically expressed CONSTANS ( CO ) is required for the activation of FLOWERING LOCUS T ( FT ), resulting in the initiation of flowering. Phytochrome A and cryptochrome photoreceptors stabilize CO in the evening by attenuating the activity of the CONSTITUTIVE PHOTOMORPHOGENIC 1– SUPPRESSOR OF PHYA ‐105 1 ( COP 1– SPA 1) ubiquitin ligase complex, which promotes turnover of CO . In contrast, phytochrome B (phyB) facilitates degradation of CO in the morning and delays flowering. Accordingly, flowering is accelerated in phyB mutants. Paradoxically, plants overexpressing phyB also show early flowering, which may arise from an early phase of rhythmic CO expression. Here we demonstrate that overexpression of phyB induces FT transcription at dusk and in the night without affecting the phase or level of CO transcription. This response depends on the light‐activated Pfr form of phyB that inhibits the function of the COP 1– SPA 1 complex by direct interactions. Our data suggest that attenuation of COP 1 activity results in the accumulation of CO protein and subsequent induction of FT . We show that phosphorylation of Ser‐86 inhibits this function of phyB by accelerating dark reversion and thus depletion of Pfr forms in the night. Our results explain the early flowering phenotype of phyB overexpression and reveal additional features of the molecular machinery by which photoreceptors mediate photoperiodism.