HOS15 represses flowering by promoting GIGANTEA degradation in response to low temperature in Arabidopsis

Flowering is the primary stage of the plant developmental transition and is tightly regulated by environmental factors such as light and temperature. However, the mechanisms by which temperature signals are integrated into the photoperiodic flowering pathway are still poorly understood. Here, we demonstrate that HOS15, which is known as a GI transcriptional repressor in the photoperiodic flowering pathway, controls flowering time in response to low ambient temperature. At 16°C, the hos15 mutant exhibits an early flowering phenotype, and HOS15 acts upstream of photoperiodic flowering genes (GI, CO, and FT). GI protein abundance is increased in the hos15 mutant and is insensitive to the proteasome inhibitor MG132. Furthermore, the hos15 mutant has a defect in low ambient temperature–mediated GI degradation, and HOS15 interacts with COP1, an E3 ubiquitin ligase for GI degradation. Phenotypic analyses of the hos15 cop1 double mutant revealed that repression of flowering by HOS15 is dependent on COP1 at 16°C. However, the HOS15–COP1 interaction was attenuated at 16°C, and GI protein abundance was additively increased in the hos15 cop1 double mutant, indicating that HOS15 acts independently of COP1 in GI turnover at low ambient temperature. This study proposes that HOS15 controls GI abundance through multiple modes as an E3 ubiquitin ligase and transcriptional repressor to coordinate appropriate flowering time in response to ambient environmental conditions such as temperature and day length. Flowering time is tightly regulated by multiple pathways. This study shows that HOS15 accelerates low ambient temperature–mediated GI degradation. HOS15 integrates photoperiodic and thermosensory flowering pathways by controlling GI abundance as an E3 ubiquitin ligase and transcriptional repressor to coordinate appropriate flowering time.