Abstract
CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) functions as an E3 ubiquitin ligase in both plants and animals. In dark-grown Arabidopsis thaliana seedlings, COP1 targets photomorphogenesis-promoting factors for degradation to repress photomorphogenesis. Little is known, however, about how COP1 itself is regulated. Here, we identify COP1 SUPPRESSOR1 (CSU1), a RING-finger E3 ubiquitin ligase, as a regulator of COP1. Genetic evidence demonstrates that csu1 mutations suppress cop1-6 phenotypes completely in the dark. Furthermore, CSU1 colocalizes with COP1 in nuclear speckles and negatively regulates COP1 protein accumulation in darkness. CSU1 can ubiquitinate COP1 in vitro and is essential for COP1 ubiquitination in vivo. Therefore, we conclude that CSU1 plays a major role in maintaining COP1 homeostasis by targeting COP1 for ubiquitination and degradation in dark-grown seedlings.
Highlights
In the dark and light, plants undergo two distinct developmental programs
We show that COP1 SUPPRESSOR1 (CSU1) colocalizes with CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) in the nucleus in plant cells
In response to FR and R light, PIF3 protein was degraded in both wild-type and csu1 mutant seedlings (Supplemental Figure 7). All these results indicate that mutation of CSU1 did not change the protein levels of COP1, HY5, phytochrome A (phyA), phyB, or PIF3 in the light
Summary
In the dark and light, plants undergo two distinct developmental programs. The dark developmental program, known as etiolation or skotomorphogenesis, allows seedlings to penetrate soil and reach the surface, where photoautotrophic growth can commence. Upon reaching light, seedling development switches to photomorphogenesis, a phase characterized by the inhibition of hypocotyl elongation, expansion of the cotyledons, and acquisition of photosynthetic capacity (Sullivan and Deng, 2003). Light perceived by photoreceptors induces a cascade resulting in massive transcriptional reprogramming (Ma et al, 2001). Forward genetic screens have identified a group of loss-of-function mutants that display photomorphogenic growth, even in darkness. The recessive nature of these cop/det/fus mutants indicates that COP/DET/FUS proteins function to suppress deetiolation in the
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