HYPK Interacts with COP1 and Enhances Its Activity to Repress Photomorphogenesis in Arabidopsis

Abstract Plants sense light through photoreceptors to switch from skotomorphogenesis in darkness to photomorphogenesis upon light exposure. This transition is centrally governed by the CONSTITUTIVE PHOTOMORPHOGENESIS1 (COP1)/SUPPRESSOR OF PHYA-105 (SPA) E3 ubiquitin ligase complex, which targets photomorphogenesis-promoting factors like ELONGATED HYPOCOTYL5 (HY5) for degradation in darkness. This study identifies Huntingtin Yeast Partner K (HYPK) as a novel negative regulator of photomorphogenesis in Arabidopsis thaliana. HYPK functions in signaling pathways mediated by multiple photoreceptors, and its protein is stabilized by light. We demonstrate that HYPK physically interacts with the central repressor COP1 and enhances its E3 ubiquitin ligase activity towards the positive regulator HY5, thereby promoting HY5 degradation. Genetic analyses reveal that HYPK and COP1 synergistically repress photomorphogenesis largely through HY5. Furthermore, HYPK modulates the nuclear dynamics of COP1, facilitating the formation and maintenance of nuclear bodies in darkness. HYPK also regulates light-induced phytochrome B (phyB) nuclear localization and photobody organization. Moreover, HYPK differentially modulates the physical interactions of COP1 with its key binding partners phyB and SPA1. Our findings establish HYPK as a critical component that integrates photoreceptor signaling with COP1 activity by both enhancing its E3 ligase function and orchestrating the nuclear dynamics of core light signaling components.