COP1 SUPPRESSOR 6 promotes photomorphogenesis by repressing the transcription and activity of PIF4 and PIF5
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ABSTRACT:
PROVIDER: PRJNA831423 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18906256_1.fastq.gz | Fastqsanger.gz | |||
| SRR18906256_2.fastq.gz | Fastqsanger.gz | |||
| SRR18906257_1.fastq.gz | Fastqsanger.gz | |||
| SRR18906257_2.fastq.gz | Fastqsanger.gz | |||
| SRR18906258_1.fastq.gz | Fastqsanger.gz |
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Project description:Light signaling precisely controls the photomorphogenic development in plants. In this study, we report COP1 SUPPRESSOR 6 (CSU6) function as positive regulator of light signaling. Loss of CSU6 function largely rescued the cop1-6 constitutively photomorphogenic phenotype. The hypocotyl length of csu6 mutant seedlings was shorter in the dark, but longer than that of wide-type in the light. CSU6 not only associated with the promoter regions of PIF4 and PIF5 to inhibit their expression during the day, but also directly interacts with both PIF4 and PIF5 to repress their transcriptional activity. CSU6 negatively controls a large group of PIF4- and PIF5-mediated genes' expression. Mutations in PIF4 and/or PIF5 are epistatic to the loss of CSU6, suggesting that CSU6 acts upstream of PIF4 and PIF5. Taken together, CSU6 promotes photomorphogenesis by negatively regulating PIF4 and PIF5 transcription and biochemical activity.
2024-04-23 | GSE201389 | GEO
Project description:Intron retention (IR) is the most common alternative splicing (AS) event in Arabidopsis. Increasing studies have demonstrated a major role of IR in gene expression regulation. The impacts of IR on plant growth and development, and response to environments remains under explored. Here, we found that IR functions directly in gene expression regulation on a genome-wide scale through detainment of the intron-retained transcripts (IRTs) in the nucleus. Through this mechanism, nuclear-retained IRTs can be kept away from translation. COP1-dependent light modulation of IRTs of light signaling genes, such as PIF4, RVE1, and ABA3, contribute to seedling morphological development in responding to changing light conditions. Further, light-induced IR changes are under the control of the spliceosome, and in part through COP1-dependent ubiquitination and degradation of DCS1, a plant-specific spliceosomal component. Our data suggests that light regulates the activity of the spliceosome and the consequent IRTs nucleus detainment to modulate photomorphogenesis through COP1.
2024-05-20 | PXD043190 | Pride
Project description:CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) and DE-ETIOLATED 1 (DET1) are founding components of two central repressor complexes of photomorphogenesis that trigger the degradation of a larger number of photomorphogenic-promoting factors in darkness. Here, we identify COP1 SUPPRESSOR 4 (CSU4) as a genetic suppressor of the cop1-6 mutation. Mutations in CSU4 largely rescued the constitutively photomorphogenic phenotype of cop1-6 and det1-1 in darkness. Loss of CSU4 function resulted in significantly longer hypocotyl in the light. Further biochemical studies revealed that CSU4 physically interacts with CIRCADIAN CLOCK-ASSOCIATED 1 (CCA1) and negatively regulates its transcriptional repression activity toward its targets. CSU4 represses the expression of CCA1 in the early morning and of PHYTOCHROME INTERACTING FACTOR 4 (PIF4) in the early evening. Our study suggests that CSU4 acts as a negative regulator of CCA1 via physically associating with CCA1, which in turn, likely serves to repress expression of CCA1 and PIF4 to promote photomorphogenesis.
| S-EPMC6233069 | biostudies-other
Project description:Light is a major determinant of plant growth and survival. NONEXPRESSER OF PATHOGENESIS-RELATED GENES 1 (NPR1) acts as a receptor for salicylic acid (SA) and serves as the key regulator of SA-mediated immune responses. However, the mechanisms by which plants integrate light and SA signals in response to environmental changes, as well as the role of NPR1 in regulating plant photomorphogenesis, remain poorly understood. This study shows that SA promotes plant photomorphogenesis by regulating PHYTOCHROME INTERACTING FACTOR 4 (PIF4). Specifically, NPR1 promotes photomorphogenesis under blue light by facilitating the degradation of PIF4 through light-induced polyubiquitination. NPR1 acts as a substrate adaptor for the CULLIN3-based E3 ligase, which ubiquitinates PIF4 at Lys129, Lys252, and Lys428, and leading to PIF4 degradation via the 26S proteasome pathway. Genetically, PIF4 is epistatic to NPR1 in the regulation of blue light-–induced photomorphogenesis, suggesting it acts downstream of NPR1. Furthermore, cryptochromes mediate the polyubiquitination of PIF4 by NPR1 in response to blue light by promoting the interaction and ubiquitination between NPR1 and PIF4. Transcriptome analysis revealed that, under blue light, NPR1 and PIF4 coordinately regulate numerous downstream genes related to light and auxin signaling pathways. Overall, these findings unveil a role for NPR1 in photomorphogenesis, highlighting a mechanism for post-translational regulation of PIF4 in response to blue light. This mechanism plays a pivotal role in the fine-tuning of plant development, enabling plants to adapt to complex environmental changes.
2024-11-26 | GSE268390 | GEO
Project description:CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) mediates various cellular and physiological processes in plants by targeting a large number of substrates for ubiquitination and degradation. In this study, we reveal that a substitution of Pro for Leu at the site of 409 in COP1 SUPPRESSOR 5 (CSU5, also called WRKY32) largely suppresses the short hypocotyls and expanded cotyledon phenotypes of cop1-6. CSU5P409L promotes the hypocotyl growth and inhibits the opening of cotyledons in plants. Loss of CSU5 function mutant seedlings display elongated hypocotyls, whereas overexpression of CSU5 leads to shortened hypocotyls. CSU5 directly associates with the promoter regions of HY5 to activate its transcription. Although COP1 interacts with both CSU5 and CSU5P409L, it negatively controls the stability of CSU5, but not CSU5P409L. CSU5P409L exhibits enhanced DNA binding ability and affects the expression of more genes compared with CSU5. Our results not only reveal the molecular role for CSU5 in promoting photomorphogenesis, but also provide insights into manipulating plant growth by engineering key components of light signaling.
2022-08-23 | GSE183463 | GEO
Project description:DE-ETIOLATED1 (DET1) is a negative regulator of plant photomorphogenesis acting as a component of the C3D complex, which can further associate to CULLIN4 to form a CRL4C3D E3 ubiquitin ligase. CRL4C3D is thought to act together with CRL4COP1SPA ubiquitin ligase, to promote the ubiquitin-mediated degradation of the master regulatory transcription factor ELONGATED HYPOCOTYL5 (HY5), thereby controlling photomorphogenic gene regulatory networks. Yet, functional links between COP1 and DET1 have long remained elusive. Here, upon mass spectrometry identification of DET1 and COP1-associated proteins, we provide in vivo evidence that DET1 associates with COP1 to promote its destabilization, a process necessary to dampen HY5 protein abundance. By regulating HY5 over-accumulation, DET1 is critical to avoid its association to second-site loci, including many PIF3 target genes. Accordingly, excessive HY5 levels result in an increased HY5 repressive activity and are sufficient to trigger fusca-like phenotypes otherwise observed typically in COP1 and COP9 signalosome mutant seedlings. This study therefore identifies that DET1-mediated regulation of COP1 stability tunes down HY5 cistrome and avoids hyper-photomorphogenic responses that might compromise plant viability.
2021-09-09 | GSE155147 | GEO
Project description:Light-induced phosphorylation is necessary and essential for the degradation of phytochrome-interacting factors (PIFs), the central repressors of photomorphogenesis. Although the kinases responsible for PIF phosphorylation have been extensively studied, the phosphatases underlying PIF dephosphorylation are largely unknown. Here, we real that mutation of FyPP1 and FyPP3, two catalytic subunits of PP6 phosphatases, promoted photomorphogenesis of seedlings in the dark. PP6 and PIFs functioned synergistically to repress photomorphogenesis. FyPP1 and FyPP3 directly interacted with and dephosphorylated PIF3 and PIF4. The light-induced degradation of PIF4 and the PIF transcriptional activities were dependent on PP6 activity. These data demonstrate that PP6 phosphatases repress photomorphogenesis through regulation of PIF phosphorylation, protein stability and transcriptional activity.
2019-09-04 | GSE128498 | GEO
Project description:Light is an environmental factor that influences various aspects of plant development. Phytochromes (phys) as light sensors regulate myriads of downstream genes in response to changes in environmental factors. VIL1 (VIN3-LIKE 1)/VERNALIZATION 5 (VRN5), a Polycomb Repressive Complex 2 (PRC2) - associated protein, mediates vernalization pathway. VIL1 directly interacts with phyB and regulates photomorphogenesis through the formation of repressive chromatin loops at downstream growth-promoting genes in response to light. CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) is an E3 ligase for a number of substrates in light signaling, acting as a central repressor of photomorphogenesis. Here, we show that VIL1 is a substrate of COP1 and COP1 degrades VIL1 through the ubiquitin/26S proteosome system (UPS) in the dark. Our study illustrates that COP1 controls light-dependent formation of chromatin loop by regulating the stability of VIL1 and limits a repressive histone modification to fine-tune expressions of growth-promoting genes during photomorphogenesis. We performed Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modifications H3K27me3 in five Arabidopsis genotypes (Col-0, vil1-1, cop1-4, vil1-1cop1-4 and hy5-215).
2024-03-06 | GSE233271 | GEO
Project description:Light is an environmental factor that influences various aspects of plant development. Phytochromes (phys) as light sensors regulate myriads of downstream genes in response to changes in environmental factors. VIL1 (VIN3-LIKE 1)/VERNALIZATION 5 (VRN5), a Polycomb Repressive Complex 2 (PRC2) - associated protein, mediates vernalization pathway. VIL1 directly interacts with phyB and regulates photomorphogenesis through the formation of repressive chromatin loops at downstream growth-promoting genes in response to light. CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) is an E3 ligase for a number of substrates in light signaling, acting as a central repressor of photomorphogenesis. Here, we show that VIL1 is a substrate of COP1 and COP1 degrades VIL1 through the ubiquitin/26S proteosome system (UPS) in the dark. Our study illustrates that COP1 controls light-dependent formation of chromatin loop by regulating the stability of VIL1 and limits a repressive histone modification to fine-tune expressions of growth-promoting genes during photomorphogenesis. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different genotypes at two time points (ZT0 and ZT6).
2024-03-06 | GSE233272 | GEO
Project description:NPR1 promotes blue light–induced plant photomorphogenesis by ubiquitinating and degrading PIF4
| PRJNA1117018 | ENA