DET1-mediated COP1 regulation avoids HY5 activity over second-site gene targets to tune plant photomorphogenesis

Abstract

DE-ETIOLATED 1 (DET1) and CONSTITUTIVE PHOTOMORPHOGENESIS 1 (COP1) are two essential repressors of Arabidopsis photomorphogenesis. These proteins can associate with CULLIN4 to form independent CRL4-based E3 ubiquitin ligases that mediate the degradation of several photomorphogenic transcription factors, including ELONGATED HYPOCOTYL 5 (HY5), thereby controlling multiple gene-regulatory networks. Despite extensive biochemical and genetic analyses of their multi-subunit complexes, the functional links between DET1 and COP1 have long remained elusive. Here, we report that DET1 associates with COP1 in vivo, enhances COP1-HY5 interaction, and promotes COP1 destabilization in a process that dampens HY5 protein abundance. By regulating its accumulation, DET1 avoids HY5 association with hundreds of second-site genomic loci, which are also frequently targeted by the skotomorphogenic transcription factor PHYTOCHROME-INTERACTING FACTOR 3. Accordingly, ectopic HY5 chromatin enrichment favors local gene repression and can trigger fusca-like phenotypes. This study therefore shows that DET1-mediated regulation of COP1 stability tunes down the HY5 cistrome, avoiding hyper-photomorphogenic responses that might compromise plant viability.

Keywords: COP1; DET1; HY5; fusca; light signaling; photomorphogenesis.