Abstract
The timing of flowering is coordinated by a web of gene regulatory networks that integrates developmental and environmental cues in plants. Light and temperature are two major environmental determinants that regulate flowering time. Although prolonged treatment with low nonfreezing temperatures accelerates flowering by stable repression of FLOWERING LOCUS C (FLC), repeated brief cold treatments delay flowering. Here, we report that intermittent cold treatments trigger the degradation of CONSTANS (CO), a central activator of photoperiodic flowering; daily treatments caused suppression of the floral integrator FLOWERING LOCUS T (FT) and delayed flowering. Cold-induced CO degradation is mediated via a ubiquitin/proteasome pathway that involves the E3 ubiquitin ligase HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE 1 (HOS1). HOS1-mediated CO degradation occurs independently of the well established cold response pathways. It is also independent of the light signaling repressor CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) E3 ligase and light wavelengths. CO has been shown to play a key role in photoperiodic flowering. Here, we demonstrated that CO served as a molecular hub, integrating photoperiodic and cold stress signals into the flowering genetic pathways. We propose that the HOS1-CO module contributes to the fine-tuning of photoperiodic flowering under short term temperature fluctuations, which often occur during local weather disturbances.
Highlights
Cold Stress Disrupts Rhythmic Expression of FLOWERING LOCUS T (FT)—Intermittent cold is frequently employed to define the effects of cold stress on the timing of flowering in Arabidopsis, because it profoundly delays flowering without plant growth alterations [28, 29]
We suspected that a floral regulatory mechanism other than FLOWERING LOCUS C (FLC) would rapidly respond to cold stress imposed by intermittent cold treatments in flowering time control
To obtain clues as to how cold stress influences flowering time at the molecular level, we systematically examined the effects of intermittent cold on the expression of flowering genes by exposing Col-0 plants to 4 °C for 6 h between ZT10 and ZT16 under long days (LDs)
Summary
The rhythmic light signals generated by the clock are mediated by GIGANTEA (GI) and CONSTANS (CO) to regulate floral integrators, such as FLOWERING LOCUS T (FT) and SUPPRESSOR OF EXPRESSION OF CO 1 (SOC1), constituting the photoperiodic flowering pathway [1, 2]. The previous studies indicate that FLC plays a critical role in the signaling cross-link between flowering timing and the cold stress response. It remain largely unknown how the flowering genetic pathways are interrelated with cold stress responses and whether FLC is a sole regulator in this process. CO was degraded through an HOS1-mediated ubiquitination mechanism, causing suppression of FT and delaying flowering. Our data support that CO acts as a molecular link that integrates cold signals into the photoperiodic flowering pathway, providing an adaptive strategy that prevents precocious flowering under fluctuating temperature conditions
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