Photoperiod sensing system for timing of flowering in plants

Abstract

CONSTANS (CO) induces the expression of FLOWERING LOCUS T (FT) in the photoperiodic pathway, and thereby regulates the seasonal timing of flowering. CO expression is induced and CO protein is stabilized by FLAVIN-BINDING KELCH REPEAT F-BOX PROTEIN 1 (FKF1) in the late afternoon, while CO is degraded by CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) during the night. These regulatory cascades were thought to act independently. In our study, we investigated the relationship between FKF1 and COP1 in the regulation of CO stability in response to ambient light conditions. A genetic analysis revealed that FKF1 acts as a direct upstream negative regulator of COP1, in which cop1 mutation is epistatic to fkf1 mutation in the photoperiodic regulation of flowering. COP1 activity requires the formation of a hetero-tetramer with SUPPRESSOR OF PHYA-105 (SPA1), [(COP1)2(SPA1)2]. Light-activated FKF1 has an increased binding capacity for COP1, forming a FKF1-COP1 hetero-dimer, and inhibiting COP1 homo-dimerization at its coiled-coil (CC) domain. Mutations in the CC domain result in poor COP1 dimerization and misregulation of photoperiodic floral induction. We propose that FKF1 represses COP1 activity by inhibiting COP1 dimerization in the late afternoon under long-day conditions, resulting in early flowering. [BMB Reports 2018; 51(4): 163-164].

Diagram 1

Possible model of the FKF1-COP1-CO regulatory module in the photoperiod-dependent induction of flowering. The blue-light receptor FKF1 is highly expressed at ZT14 – ZT16, at which time the plants are exposed to light under LD conditions (16 h light/day), but are in the dark under SD (8 h light/day) conditions. Another blue-light receptor, CRY2, is stabilized in light, but quickly destabilized in darkness. In LD conditions, the light-activated blue-light receptors FKF1 and CRY2 interact with the COP1-SPA1 complexes, forming FKF1-COP1 and CRY2-SPA1 complexes. This might inhibit the formation of the COP1-SPA1 complexes in the late afternoon, resulting in the inactivation of COP1 or the destabilization of the COP1-SPA1 complex. Inhibition of COP1-SPA1 complex formation increases CO protein stability in the late afternoon, enabling it to interact with FKF1 and induce FT transcription for floral induction. In SD conditions, both CO and FKF1 are expressed in the dark, and CRY2 is destabilized in the dark. Thus, the blue-light receptors FKF1 and CRY2 are present in their inactive forms in darkness, and cannot destabilize COP1 complex, resulting in the rapid breakdown of CO by ubiquitin-dependent proteolysis.