Arabidopsis RUP2 represses UVR8-mediated flowering in noninductive photoperiods.

Plants have evolved complex photoreceptor-controlled mechanisms to sense and respond to seasonal changes in day length. This ability allows plants to optimally time the transition from vegetative growth to flowering. UV-B is an important part intrinsic to sunlight; however, whether and how it affects photoperiodic flowering has remained elusive. Here, we report that, in the presence of UV-B, genetic mutation of REPRESSOR OF UV-B PHOTOMORPHOGENESIS 2 (RUP2) renders the facultative long day plant Arabidopsis thaliana a day-neutral plant and that this phenotype is dependent on the UV RESISTANCE LOCUS 8 (UVR8) UV-B photoreceptor. We provide evidence that the floral repression activity of RUP2 involves direct interaction with CONSTANS, repression of this key activator of flowering, and suppression of FLOWERING LOCUS T transcription. RUP2 therefore functions as an essential repressor of UVR8-mediated induction of flowering under noninductive short day conditions and thus provides a crucial mechanism of photoperiodic flowering control.

Dissecting the functions of COP1 in the UVR8 pathway with a COP1 variant in Arabidopsis.

COP1 is a critical repressor of plant photomorphogenesis in darkness. However, COP1 plays distinct roles in the photoreceptor UVR8 pathway in Arabidopsis thaliana. COP1 interacts with ultraviolet B (UV-B)-activated UVR8 monomers and promotes their retention and accumulation in the nucleus. Moreover, COP1 has a function in UV-B signaling, which involves the binding of its WD40 domain to UVR8 and HY5 via conserved Val-Pro (VP) motifs of these proteins. UV-B-activated UVR8 interacts with COP1 via both the core domain and the VP motif, leading to the displacement of HY5 from COP1 and HY5 stabilization. However, it remains unclear whether the function of COP1 in UV-B signaling is solely dependent on its VP motif binding capacity and whether UV-B regulates the subcellular localization of COP1. Based on published structures of the COP1 WD40 domain, we generated a COP1 variant with a single amino acid substitution, COP1C509S , which cannot bind to VP motifs but retains the ability to interact with the UVR8 core domain. UV-B only marginally increased nuclear YFP-COP1 levels and significantly promoted YFP-COP1 accumulation in the cytosol, but did not exert the same effects on YFP-COP1C509S . Thus, the full UVR8-COP1 interaction is important for COP1 accumulation in the cytosol. Notably, UV-B signaling including activation of HY5 transcription was obviously inhibited in the Arabidopsis lines expressing YFP-COP1C509S , which cannot bind VP motifs. We conclude that the full binding of UVR8 to COP1 leads to the predominant accumulation of COP1 in the cytosol and that COP1 has an additional function in UV-B signaling besides VP binding-mediated protein destabilization.

ELONGATED HYPOCOTYL5 (HY5) and HY5 HOMOLOGUE (HYH) maintain shade avoidance suppression in UV-B.

Reductions in red to far-red ratio (R:FR) provide plants with an unambiguous signal of vegetational shade and are monitored by phytochrome photoreceptors. Plants integrate this information with other environmental cues to determine the proximity and density of encroaching vegetation. Shade-sensitive species respond to reductions in R:FR by initiating a suite of developmental adaptations termed shade avoidance. These include the elongation of stems to facilitate light foraging. Hypocotyl elongation is driven by increased auxin biosynthesis promoted by PHYTOCHROME INTERACTING FACTORs (PIF) 4, 5 and 7. UV-B perceived by the UV RESISTANCE LOCUS 8 (UVR8) photoreceptor rapidly inhibits shade avoidance, in part by suppressing PIF4/5 transcript accumulation and destabilising PIF4/5 protein. Here, we show that longer-term inhibition of shade avoidance is sustained by ELONGATED HYPOCOTYL 5 (HY5) and HY5 HOMOLOGUE (HYH), which regulate transcriptional reprogramming of genes involved in hormone signalling and cell wall modification. HY5 and HYH are elevated in UV-B and suppress the expression of XYLOGLUCAN ENDOTRANSGLUCOSYLASE/HYDROLASE (XTH) genes involved in cell wall loosening. They additionally increase expression GA2-OXIDASE1 (GA2ox1) and GA2ox2, encoding gibberellin catabolism enzymes that act redundantly to stabilise the PIF-inhibiting DELLA proteins. UVR8 therefore regulates temporally distinct signalling pathways to first rapidly inhibit and subsequently maintain suppression of shade avoidance following UV-B exposure.

UV-B photoreceptor UVR8 interacts with MYB73/MYB77 to regulate auxin responses and lateral root development.

The UV-B photoreceptor UVR8 mediates multiple UV-B responses in plants, but the function of UVR8 in regulating root development has not previously been investigated. Here, we show that UV-B light inhibits Arabidopsis lateral root growth in a UVR8-dependent manner. Monomeric UVR8 inhibits auxin responses in a tissue-autonomous manner and thereby regulates lateral root growth. Genome-wide gene expression analysis demonstrated that auxin and UV-B irradiation antagonistically regulate auxin-regulated gene expression. We further show that UVR8 physically interacts with MYB73/MYB77 (MYB DOMAIN PROTEIN 73/77) in a UV-B-dependent manner. UVR8 inhibits lateral root development via regulation of MYB73/MYB77. When activated by UV-B light, UVR8 localizes to the nucleus and inhibits the DNA-binding activities of MYB73/MYB77 and directly represses the transcription of their target auxin-responsive genes. Our results demonstrate that UV-B light and UVR8 are critical for both shoot morphogenesis and root development. The UV-B-dependent interaction of UVR8 and MYB73/MYB77 serves as an important module that integrates light and auxin signaling and represents a new UVR8 signaling mechanism in plants.

A UVB-responsive common variant at chromosome band 7p21.1 confers tanning response and melanoma risk via regulation of the aryl hydrocarbon receptor, AHR.

Genome-wide association studies (GWASs) have identified a melanoma-associated locus on chromosome band 7p21.1 with rs117132860 as the lead SNP and a secondary independent signal marked by rs73069846. rs117132860 is also associated with tanning ability and cutaneous squamous cell carcinoma (cSCC). Because ultraviolet radiation (UVR) is a key environmental exposure for all three traits, we investigated the mechanisms by which this locus contributes to melanoma risk, focusing on cellular response to UVR. Fine-mapping of melanoma GWASs identified four independent sets of candidate causal variants. A GWAS region-focused Capture-C study of primary melanocytes identified physical interactions between two causal sets and the promoter of the aryl hydrocarbon receptor (AHR). Subsequent chromatin state annotation, eQTL, and luciferase assays identified rs117132860 as a functional variant and reinforced AHR as a likely causal gene. Because AHR plays critical roles in cellular response to dioxin and UVR, we explored links between this SNP and AHR expression after both 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and ultraviolet B (UVB) exposure. Allele-specific AHR binding to rs117132860-G was enhanced following both, consistent with predicted weakened AHR binding to the risk/poor-tanning rs117132860-A allele, and allele-preferential AHR expression driven from the protective rs117132860-G allele was observed following UVB exposure. Small deletions surrounding rs117132860 introduced via CRISPR abrogates AHR binding, reduces melanocyte cell growth, and prolongs growth arrest following UVB exposure. These data suggest AHR is a melanoma susceptibility gene at the 7p21.1 risk locus and rs117132860 is a functional variant within a UVB-responsive element, leading to allelic AHR expression and altering melanocyte growth phenotypes upon exposure.

Making the most of canopy light: Shade avoidance under a fluctuating spectrum and irradiance.

In the field, plants face constantly changing light conditions caused by both atmospheric effects and neighbouring vegetation. This interplay creates a complex, fluctuating light environment within plant canopies. Shade-intolerant species rely on light cues from competitors to trigger shade avoidance responses, ensuring access to light for photosynthesis. While research often uses controlled growth chambers with steady light to study shade avoidance responses, the influence of light fluctuations in real-world settings remains unclear. This review examines the dynamic light environments found in woodlands, grasslands, and crops. We explore how plants respond to some fluctuations but not others, analyse the potential reasons for these differences, and discuss the possible molecular mechanisms regulating this sensitivity. We propose that studying shade avoidance responses under fluctuating light conditions offers a valuable tool to explore the intricate regulatory network behind them.

Comparative transcriptomics elucidates the cellular responses of an aeroterrestrial zygnematophyte to UV radiation.

The zygnematophytes are the closest relatives of land plants and comprise several lineages that adapted to a life on land. Species of the genus Serritaenia form colorful, mucilaginous capsules, which surround the cells and block harmful solar radiation, one of the major terrestrial stressors. In eukaryotic algae, this 'sunscreen mucilage' represents a unique photoprotective strategy, whose induction and chemical background are unknown. We generated a de novo transcriptome of Serritaenia testaceovaginata and studied its gene regulation under moderate UV radiation (UVR) that triggers sunscreen mucilage under experimental conditions. UVR induced the repair of DNA and the photosynthetic apparatus as well as the synthesis of aromatic specialized metabolites. Specifically, we observed pronounced expressional changes in the production of aromatic amino acids, phenylpropanoid biosynthesis genes, potential cross-membrane transporters of phenolics, and extracellular, oxidative enzymes. Interestingly, the most up-regulated enzyme was a secreted class III peroxidase, whose embryophyte homologs are involved in apoplastic lignin formation. Overall, our findings reveal a conserved, plant-like UVR perception system (UVR8 and downstream factors) in zygnematophyte algae and point to a polyphenolic origin of the sunscreen pigment of Serritaenia, whose synthesis might be extracellular and oxidative, resembling that of plant lignins.

Recent advances in UV-B signalling: interaction of proteins with the UVR8 photoreceptor.

The photoreceptor UVR8 mediates many plant responses to UV-B and short wavelength UV-A light. UVR8 functions through interactions with other proteins which lead to extensive changes in gene expression. Interactions with particular proteins determine the nature of the response to UV-B. It is therefore important to understand the molecular basis of these interactions: how are different proteins able to bind to UVR8 and how is differential binding regulated? This concise review highlights recent developments in addressing these questions. Key advances are discussed with regard to: identification of proteins that interact with UVR8; the mechanism of UVR8 accumulation in the nucleus; the photoactivation of UVR8 monomer; the structural basis of interaction between UVR8 and CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) and REPRESSOR OF UV-B PHOTOMORPHOGENESIS (RUP) proteins; the role of UVR8 phosphorylation in modulating interactions and responses to UV-B. Nevertheless, much remains to be understood and the need to extend future research to the growing list of interactors is emphasised.

Exploring the complexities of plant UV responses; distinct effects of UV-A and UV-B wavelengths on Arabidopsis rosette morphology.

UV-B radiation can substantially impact plant growth. To study UV-B effects, broadband UV-B tubes are commonly used. Apart from UV-B, such tubes also emit UV-A wavelengths. This study aimed to distinguish effects of different UV-B intensities on Arabidopsis thaliana wildtype and UVR8 mutant rosette morphology, from those by accompanying UV-A. UV-A promotes leaf-blade expansion along the proximal-distal, but not the medio-lateral, axis. Consequent increases in blade length: width ratio are associated with increased light capture. However, petiole length is not affected by UV-A exposure. This scenario is distinct from the shade avoidance driven by low red to far-red ratios, whereby leaf blade elongation is impeded but petiole elongation is promoted. Thus, the UV-A mediated elongation response is phenotypically distinct from classical shade avoidance. UV-B exerts inhibitory effects on petiole length, blade length and leaf area, and these effects are mediated by UVR8. Thus, UV-B antagonises aspects of both UV-A mediated elongation and classical shade avoidance. Indeed, this study shows that accompanying UV-A wavelengths can mask effects of UV-B. This may lead to potential underestimates of the magnitude of the UV-B induced morphological response using broadband UV-B tubes.

Expression of active caspase 3 in the rat lens after in vivo exposure to subthreshold dose of UVR-B.

PURPOSES: The aim of this study is to investigate the time evolution of active caspase 3 within first 120 h in the rat lens after in vivo exposure to subthreshold dose of UVR-B. METHODS: Twenty three six-week-old female albino Sprague-Dawley rats were exposed to subthreshold dose (1 kJ/m2) of UVR-B unilaterally and sacrificed at 24, 41, 70 and 120 h after exposure. Lenses were enucleated and active caspase 3 was detected by Western Blot. The time evolution of active caspase 3 was then plotted as a function of relative mean difference in active caspase 3 between exposed and nonexposed lenses. RESULTS: There is expression of active caspase 3 in both exposed and nonexposed lenses but there is no difference in relative mean difference in active caspase 3 between exposed and nonexposed lenses in all four postexposure groups. CONCLUSIONS: Exposure to subthreshold dose of UVR-B does not induce apoptosis in the rat lens in vivo within first 120 h though there is a non-significant increase of active caspase 3 at 120 h. Increase in sample size might reduce the variation level in expression of active caspase 3 in the rat lenses.

A revised action spectrum for vitamin D synthesis by suberythemal UV radiation exposure in humans in vivo.

Action spectra are important biological weighting functions for risk/benefit analyses of ultraviolet (UV) radiation (UVR) exposure. One important human benefit of exposure to terrestrial solar UVB radiation (∼295 to 315 nm) is the cutaneous synthesis of vitamin D3 that is initiated by the photoconversion of 7-dehydrocholesterol to previtamin D3 An action spectrum for this process that is followed by other nonphotochemical steps to achieve biologically active vitamin D3 has been established from ex vivo data and is widely used, although its validity has been questioned. We tested this action spectrum in vivo by full- or partial-body suberythemal irradiation of 75 healthy young volunteers with five different polychromatic UVR spectra on five serial occasions. Serum 25-hydroxyvitamin D3 [25(OH)D3] levels, as the most accurate measure of vitamin D3 status, were assessed before, during, and after the exposures. These were then used to generate linear dose-response curves that were different for each UVR spectrum. It was established that the previtamin D3 action spectrum was not valid when related to the serum 25(OH)D3 levels, as weighting the UVR doses with this action spectrum did not result in a common regression line unless it was adjusted by a blue shift, with 5 nm giving the best fit. Such a blue shift is in accord with the published in vitro action spectra for vitamin D3 synthesis. Thus, calculations regarding the risk (typically erythema) versus the benefit of exposure to solar UVR based on the ex vivo previtamin D3 action spectrum require revision.

Dermatologic Manifestations of Mitochondrial Dysfunction: A Review of the Literature.

Mitochondria are eukaryotic cellular organelles that function in energy metabolism, ROS production, and programmed cell death. Cutaneous epithelial and hair follicle dermal papilla cells are energy-rich cells that thereby may be affected by mitochondrial dysfunction and DNA mutation accumulation. In this review, we aimed to summarize the medical literature assessing dermatologic conditions and outcomes associated with mitochondrial dysfunction. A search of PubMed and Embase was performed with subsequent handsearching to retrieve additional relevant articles. Mitochondrial DNA (mtDNA) deletions, mutation accumulation, and damage are associated with phenotypic signs of cutaneous aging, hair loss, and impaired wound healing. In addition, several dermatologic conditions are associated with aberrant mitochondrial activity, such as systemic lupus erythematosus, psoriasis, vitiligo, and atopic dermatitis. Mouse model studies have better established causality between mitochondrial damage and dermatologic outcomes, with some depicting reversibility upon restoration of mitochondrial function. Mitochondrial function mediates a variety of dermatologic conditions, and mitochondrial components may be a promising target for therapeutic strategies.

1,25-Dihydroxyvitamin D3 Suppresses UV-Induced Poly(ADP-Ribose) Levels in Primary Human Keratinocytes, as Detected by a Novel Whole-Cell ELISA.

Photoprotective properties of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) to reduce UV-induced DNA damage have been established in several studies. UV-induced DNA damage in skin such as single or double strand breaks is known to initiate several cellular mechanisms including activation of poly(ADP-ribose) (pADPr) polymerase-1 (PARP-1). DNA damage from UV also increases extracellular signal-related kinase (ERK) phosphorylation, which further increases PARP activity. PARP-1 functions by using cellular nicotinamide adenine dinucleotide (NAD+) to synthesise pADPr moieties and attach these to target proteins involved in DNA repair. Excessive PARP-1 activation following cellular stress such as UV irradiation may result in excessive levels of cellular pADPr. This can also have deleterious effects on cellular energy levels due to depletion of NAD+ to suboptimal levels. Since our previous work indicated that 1,25(OH)2D3 reduced UV-induced DNA damage in part through increased repair via increased energy availability, the current study investigated the effect of 1,25(OH)2D3 on UV-induced PARP-1 activity using a novel whole-cell enzyme- linked immunosorbent assay (ELISA) which quantified levels of the enzymatic product of PARP-1, pADPr. This whole cell assay used around 5000 cells per replicate measurement, which represents a 200-400-fold decrease in cell requirement compared to current commercial assays that measure in vitro pADPr levels. Using our assay, we observed that UV exposure significantly increased pADPr levels in human keratinocytes, while 1,25(OH)2D3 significantly reduced levels of UV-induced pADPr in primary human keratinocytes to a similar extent as a known PARP-1 inhibitor, 3-aminobenzamide (3AB). Further, both 1,25(OH)2D3 and 3AB as well as a peptide inhibitor of ERK-phosphorylation significantly reduced DNA damage in UV-exposed keratinocytes. The current findings support the proposal that reduction in pADPr levels may be critical for the function of 1,25(OH)2D3 in skin to reduce UV-induced DNA damage.

The Skin-Brain Axis: From UV and Pigmentation to Behaviour Modulation.

The skin-brain axis has been suggested to play a role in several pathophysiological conditions, including opioid addiction, Parkinson's disease and many others. Recent evidence suggests that pathways regulating skin pigmentation may directly and indirectly regulate behaviour. Conversely, CNS-driven neural and hormonal responses have been demonstrated to regulate pigmentation, e.g., under stress. Additionally, due to the shared neuroectodermal origins of the melanocytes and neurons in the CNS, certain CNS diseases may be linked to pigmentation-related changes due to common regulators, e.g., MC1R variations. Furthermore, the HPA analogue of the skin connects skin pigmentation to the endocrine system, thereby allowing the skin to index possible hormonal abnormalities visibly. In this review, insight is provided into skin pigment production and neuromelanin synthesis in the brain and recent findings are summarised on how signalling pathways in the skin, with a particular focus on pigmentation, are interconnected with the central nervous system. Thus, this review may supply a better understanding of the mechanism of several skin-brain associations in health and disease.

UVR8-TCP4-LOX2 module regulates UV-B tolerance in Arabidopsis.

The phytohormone jasmonate (JA) coordinates stress and growth responses to increase plant survival in unfavorable environments. Although JA can enhance plant UV-B stress tolerance, the mechanisms underlying the interaction of UV-B and JA in this response remain unknown. In this study, we demonstrate that the UV RESISTANCE LOCUS 8 - TEOSINTE BRANCHED1, Cycloidea and PCF 4 - LIPOXYGENASE2 (UVR8-TCP4-LOX2) module regulates UV-B tolerance dependent on JA signaling pathway in Arabidopsis thaliana. We show that the nucleus-localized UVR8 physically interacts with TCP4 to increase the DNA-binding activity of TCP4 and upregulate the JA biosynthesis gene LOX2. Furthermore, UVR8 activates the expression of LOX2 in a TCP4-dependent manner. Our genetic analysis also provides evidence that TCP4 acts downstream of UVR8 and upstream of LOX2 to mediate plant responses to UV-B stress. Our results illustrate that the UV-B-dependent interaction of UVR8 and TCP4 serves as an important UVR8-TCP4-LOX2 module, which integrates UV-B radiation and JA signaling and represents a new UVR8 signaling mechanism in plants.

Cysteines have a role in conformation of the UVR8 photoreceptor.

The UV RESISTANCE LOCUS 8 (UVR8) photoreceptor mediates plant responses to Ultraviolet-B (UV-B) wavelengths. The UVR8 dimer dissociates into monomers following UV-B photoreception, a process accompanied by conformational changes that facilitate interaction of UVR8 with proteins that initiate responses. However, the importance of particular amino acids in maintaining UVR8 conformation and modulating protein interactions is poorly understood. Here we examine the roles of cysteine amino acids C231 and C335 in UVR8 structure and function. UVR8C231S,C335S mutant protein forms dimers and monomerizes similarly to wild-type UVR8. UVR8C231S,C335S interacts with CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) in plants to initiate photomorphogenic responses to UV-B, although the interaction is weaker when examined in yeast two-hybrid assays. Similarly, the interaction of UVR8C231S,C335S with REPRESSOR OF UV-B PHOTOMORPHOGENESIS (RUP) proteins is weaker in both plants and yeast compared with wild-type UVR8. Re-dimerization of UVR8 in plants, which is mediated by RUP proteins, occurs with reduced efficiency in UVR8C231S,C335S . Fluorescence resonance energy transfer analysis indicates that UVR8C231S,C335S has an altered conformation in plants, in that the N- and C-termini appear closer together, which may explain the altered protein interactions.

Arabidopsis B-box transcription factors BBX20-22 promote UVR8 photoreceptor-mediated UV-B responses.

Plants undergo photomorphogenic development in the presence of light. Photomorphogenesis is repressed by the E3 ubiquitin ligase CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1), which binds to substrates through their valine-proline (VP) motifs. The UV RESISTANCE LOCUS 8 (UVR8) photoreceptor senses UV-B and inhibits COP1 through the cooperative binding of its own VP motif and photosensing core to COP1, thereby preventing COP1 binding to substrates, including the basic leucine zipper (bZIP) transcriptional regulator ELONGATED HYPOCOTYL 5 (HY5). As a key promoter of visible light and UV-B photomorphogenesis, HY5 requires coregulators for its function. The B-box family transcription factors BBX20-BBX22 were recently described as HY5 rate-limiting coactivators under red light, but their role in UVR8 signaling was unknown. Here we describe a hypermorphic bbx21-3D mutant with enhanced photomorphogenesis, carrying a proline-to-leucine mutation at position 314 in the VP motif that impairs the interaction with and regulation by COP1. We show that BBX21 and BBX22 are UVR8-dependently stabilized after UV-B exposure, which is counteracted by a repressor induced by HY5/BBX activity. bbx20 bbx21 bbx22 mutants under UV-B are impaired in hypocotyl growth inhibition, photoprotective pigment accumulation and the expression of several HY5-dependent genes under continuous UV-B, but the immediate induction of marker genes after exposure to UV-B remains surprisingly rather unaffected. We conclude that BBX20-BBX22 contribute to HY5 activity in a subset of UV-B responses, but that additional, presently unknown, coactivators for HY5 are functional in early UVR8 signaling.

A seed-specific transcription factor, HSFA9, anticipates UV-B light responses by mimicking the activation of the UV-B receptor in tobacco.

Sunflower heat shock factor A9 (HSFA9, hereafter A9) is a transcription factor involved in seed desiccation tolerance and longevity. A9 also links the regulation of seed maturation with that of seedling photomorphogenesis through visible light receptors. Analyses in transgenic Nicotiana tabacum (tobacco) indicated that A9 also affects responses mediated by NtUVR8, the receptor of ultraviolet light B (UV-B). We compared the effects of A9 and UV-B illumination on the nuclear localization of GFP-NtUVR8 in Nicotiana benthamiana leaves. We also used co-immunoprecipitation and limited proteolysis for analyzing the interaction between A9 and NtUVR8. We found that A9, by binding to NtUVR8, induced structural changes that resulted in enhancing the nuclear localization of NtUVR8 by hindering its nuclear export. The localization of UVR8 is crucial for receptor activation and function in Arabidopsis, where UV-B-activated nuclear UVR8 binds the E3 ubiquitin ligase COP1, leading to enhanced UV-B responses and photoprotection. A9 similarly activated NtUVR8 by enhancing COP1 binding without UV-B light. Seedlings and dark-germinated seeds that overexpress A9 showed primed UV-B light stress protection. Our results unveil a UV-B-independent activation mechanism and a role for UVR8 in plant seeds that might contribute to early stress protection, facilitating seedling establishment.

Genome-wide characterization of regulator of chromosome condensation 1 (RCC1) gene family in Artemisia annua L. revealed a conservation evolutionary pattern.

BACKGROUND: Artemisia annua is the major source for artemisinin production. The artemisinin content in A. annua is affected by different types of light especially the UV light. UVR8, a member of RCC1 gene family was found to be the UV-B receptor in plants. The gene structures, evolutionary history and expression profile of UVR8 or RCC1 genes remain undiscovered in A. annua. RESULTS: Twenty-two RCC1 genes (AaRCC1) were identified in each haplotype genome of two diploid strains of A. annua, LQ-9 and HAN1. Varied gene structures and sequences among paralogs were observed. The divergence of most RCC1 genes occurred at 46.7 - 51 MYA which overlapped with species divergence of core Asteraceae during the Eocene, while no recent novel RCC1 members were found in A. annua genome. The number of RCC1 genes remained stable among eudicots and RCC1 genes underwent purifying selection. The expression profile of AaRCC1 is analogous to that of Arabidopsis thaliana (AtRCC1) when responding to environmental stress. CONCLUSIONS: This study provided a comprehensive characterization of the AaRCC1 gene family and suggested that RCC1 genes were conserved in gene number, structures, constitution of amino acids and expression profiles among eudicots.

Plant photoreceptors and their signaling components compete for COP1 binding via VP peptide motifs.

Plants sense different parts of the sun's light spectrum using distinct photoreceptors, which signal through the E3 ubiquitin ligase COP1. Here, we analyze why many COP1-interacting transcription factors and photoreceptors harbor sequence-divergent Val-Pro (VP) motifs that bind COP1 with different binding affinities. Crystal structures of the VP motifs of the UV-B photoreceptor UVR8 and the transcription factor HY5 in complex with COP1, quantitative binding assays, and reverse genetic experiments together suggest that UVR8 and HY5 compete for COP1. Photoactivation of UVR8 leads to high-affinity cooperative binding of its VP motif and its photosensing core to COP1, preventing COP1 binding to its substrate HY5. UVR8-VP motif chimeras suggest that UV-B signaling specificity resides in the UVR8 photoreceptor core. Different COP1-VP peptide motif complexes highlight sequence fingerprints required for COP1 targeting. The blue-light photoreceptors CRY1 and CRY2 also compete with transcription factors for COP1 binding using similar VP motifs. Thus, our work reveals that different photoreceptors and their signaling components compete for COP1 via a conserved mechanism to control different light signaling cascades.