COP1 controls light-dependent chromatin remodeling in Arabidopsis [RNA-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA975602 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24709536_1.fastq.gz | Fastqsanger.gz | |||
| SRR24709536_2.fastq.gz | Fastqsanger.gz | |||
| SRR24709537_1.fastq.gz | Fastqsanger.gz | |||
| SRR24709537_2.fastq.gz | Fastqsanger.gz | |||
| SRR24709538_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:COP1 controls light-dependent chromatin remodeling in Arabidopsis
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Project description:COP1 controls light-dependent chromatin remodeling in Arabidopsis [ChIP-Seq]
| PRJNA975601 | ENA
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: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:This SuperSeries is composed of the SubSeries listed below.
2024-03-06 | GSE233273 | GEO
Project description:The proper accumulation of BBX22 mediated by COP1 is crucial for plants to maintain better growth fitness when growing in the dark environment as well as responding to seasonal changes in day-length. The constitutive-photomorphogenic development of the cop1 mutant is enhanced in cop1BBX22-GFPox plants, which show a short hypocotyl, high anthocyanin accumulation and expression of light-responsive genes. Target genes responsible for the exaggerated light phenotype in cop1BBX22-GFPox plants were revealed by comparing transcriptomes among dark-grown wild-type, cop1 and cop1BBX22-GFPox plants. Expression of genes regulated by light and multiple hormones are altered in plants over-accumulating BBX22, implying a coordination role of BBX22 in light- and hormone-mediated seedling development. Three biological replicates for 4-day-old etiolated seedlings of wild type (Col-0) and two mutants (cop1-4 and cop1-4BBX22-GFPox).
2011-06-01 | E-GEOD-22983 | biostudies-arrayexpress
Project description:The mRNA expression profiles of the quadruple spa mutant spaQ and cop1-4 were analyzed in 1 hour red light treated condition. Under same condition, the gene expression changes in phyB-SPA1 interaction domain mutant was analyzed and compared with wild type.
2018-07-14 | GSE117114 | GEO
Project description:In order to assess the physiological role of Cop1 in vivo we generated mice that do no longer express the protein. Cop1KO mice die at around E10.5 of embryonic development. In order to gain insights into the molecular mechanisms that cause the embryonic death we compared the genome-wide gene expression profile of E9.5 wild-tytpe and Cop1-null embryos. The data do not support a role for Cop1 in the regulation of the p53 pathway in vivo and highlight a role for Cop1 in cardiovascular development and/or angiogenesis. The abstract of the associated publication is as follows:Biochemical data have suggested conflicting roles for the E3 ubiquitin ligase Cop1 in tumourigenesis. Here we present the first in vivo investigation of the role of Cop1 in cancer aetiology. We used an innovative genetic approach to generate an allelic series of Cop1 and show that Cop1 hypomorphic mice spontaneously develop malignancy at a high frequency in their first year of life and are highly susceptible to radiation-induced lymphomagenesis. Biochemically, we show that Cop1 regulates c-Jun oncoprotein stability and modulates c-Jun/AP1 transcriptional activity in vivo. Cop1-deficiency stimulates cell proliferation in a c-Jun-dependent manner. We conclude that Cop1 is a tumour suppressor that antagonizes c-Jun oncogenic activity in vivo. RNA from 6 different control embryos (+/+ or +/-) were mixed and subdivided into control pool 1 and pool 2. RNA from 6 different Cop-null embryos were mixed and subdivided into KO pool 1 and pool 2.
2011-01-13 | E-GEOD-18636 | biostudies-arrayexpress
Project description:The proper accumulation of BBX22 mediated by COP1 is crucial for plants to maintain better growth fitness when growing in the dark environment as well as responding to seasonal changes in day-length. The constitutive-photomorphogenic development of the cop1 mutant is enhanced in cop1BBX22-GFPox plants, which show a short hypocotyl, high anthocyanin accumulation and expression of light-responsive genes. Target genes responsible for the exaggerated light phenotype in cop1BBX22-GFPox plants were revealed by comparing transcriptomes among dark-grown wild-type, cop1 and cop1BBX22-GFPox plants. Expression of genes regulated by light and multiple hormones are altered in plants over-accumulating BBX22, implying a coordination role of BBX22 in light- and hormone-mediated seedling development.
2011-06-01 | GSE22983 | GEO