Repression of light signaling by Arabidopsis SPA1 involves post‐translational regulation of HFR1 protein accumulation

Abstract

SummaryArabidopsis uses two major classes of photoreceptors to mediate seedling de-etiolation. The cryptochromes (cry1 and cry2) absorb blue/ultraviolet-A light, whereas the phytochromes (phyA-phyE) predominantly regulate responses to red/far-red light. Arabidopsis COP1 represses light signaling by acting as an E3 ubiquitin ligase in the nucleus, and is responsible for targeted degradation of a number of photomorphogenesispromoting factors, including HY5, LAF1, phyA, and HFR1. Distinct light signaling pathways initiated by multiple photoreceptors (including both phytochromes and cryptochromes) eventually converge on COP1, causing its inactivation and nuclear depletion. Arabidopsis SPA1, which encodes a protein structurally related to COP1, also represses light signaling under various light conditions. In this study, we present genetic evidence supporting that HFR1, which encodes a photomorphogenesis-promoting bHLH transcription factor, acts downstream of SPA1 and is required for different subsets of branch pathways of light signaling controlled by SPA1 under different light conditions. We show that SPA1 physically interacts with HFR1 in a yeast twohybrid assay and an in vitro co-immunoprecipitation assay. We demonstrate that higher levels of HFR1 protein accumulate in the spa1 mutant background under various light conditions, including far-red, red, blue, and white light, whereas a marginal increase in HFR1 transcript level is only seen in dark-and far-red light-grown spa1-100 mutants. Together, our data suggest that repression of light signaling by Arabidopsis SPA1 likely involves post-translational regulation of HFR1 protein accumulation.

Arabidopsis SPA proteins regulate photoperiodic flowering and interact with the floral inducer CONSTANS to regulate its stability

“…Because spa and cop1 mutations also interact genetically it is hypothesized that SPA proteins function in concert with COP1 to ubiquitinate activators of the light response (Hoecker and Quail, 2001;Laubinger et al, 2004;Saijo et al, 2003). In agreement with this idea, HY5 and HFR1 protein levels are increased in spa1 mutant seedlings (Saijo et al, 2003;Yang et al, 2005a). Moreover, recombinant SPA1 altered the in vitro ubiquitin ligase activity of COP1 (Saijo et al, 2003;Seo et al, 2003).…”

“…It has been shown previously that SPA proteins act in concert with another repressor of light signaling, the ubiquitin ligase COP1, which ubiquitinates light signaling activators in dark-grown seedlings (Hoecker and Quail, 2001;Laubinger et al, 2004;Saijo et al, 2003;Seo et al, 2003;Yang et al, 2005a). Here, we have demonstrated that SPA proteins are, moreover, required for photoperiodic flowering in the facultative LD plant Arabidopsis.…”

OWL1: An Arabidopsis J-Domain Protein Involved in Perception of Very Low Light Fluences

“…HFR1 also interacts with the myb transcription factor LONG AFTER FAR-RED LIGHT1, which is involved in FR-HIR (Jang et al, 2007). Furthermore, HFR1 interacts with COP1 and SPA1, leading to its ubiquitin-dependent degradation in darkness, thereby abolishing photomorphogenesis (Duek et al, 2004;Jang et al, 2005;Yang et al, 2005aYang et al, , 2005b. HFR1 phosphorylation is promoted by light, and the protein is stabilized under these conditions.…”

Functional Interconnection of MYC2 and SPA1 in the Photomorphogenic Seedling Development of Arabidopsis

“…Furthermore, it has been demonstrated that COP1-mediated degradation of HY5, LAF1, and HFR1 is stimulated by SUPPRES-SOR OF PHYTOCHROME A1 (SPA1), a negative regulator of photomorphogenesis (Saijo et al, 2003;Seo et al, 2003Seo et al, , 2004Jang et al, 2005;Yang and Wang, 2006). SPA1 has been shown to physically interact with COP1, HY5, and HFR1 and is required for COP1-mediated degradation of HY5 and HFR1 (Hoecker and Quail, 2001;Saijo et al, 2003;Yang et al, 2005).…”

“…Among them, COP1 is a well-studied master repressor of photomorphogenesis (Deng and Quail, 1992). COP1 functions as an E3 ubiquitin ligase in the nucleus and is responsible for the degradation of a group of photomorphogenic growth-promoting factors such as HY5, LAF1, HFR1, and phyA and thereby desensitizes light signal transduction (Osterlund et al, 2000;Saijo et al, 2003;Seo et al, 2003Seo et al, , 2004Yang et al, 2005). Furthermore, it has been demonstrated that COP1-mediated degradation of HY5, LAF1, and HFR1 is stimulated by SUPPRES-SOR OF PHYTOCHROME A1 (SPA1), a negative regulator of photomorphogenesis (Saijo et al, 2003;Seo et al, 2003Seo et al, , 2004Jang et al, 2005;Yang and Wang, 2006).…”