Phytochrome B-SPA-COP1 regulation of red light induced gene expressions in Arabidopsis thaliana
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE117114 | GEO | 2018/07/14
REPOSITORIES: GEO
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Project description:The mRNA expression profiles of WT and the quadruple spa mutant spaQ were analyzed in 24 hour 22degC and 28degC treated condition. The gene expression changes was analyzed and compared within 22degC and 28degC.
2020-09-29 | GSE142354 | GEO
Project description:The total mRNA and polysomal RNA expression profiles of wild type (Col-0) and the quadruple spa mutant (spaQ) were analyzed under dark or in 4 hour light treated condition. The gene expression changed in spaQ mutant was analyzed and compared with Col-0.
2024-03-10 | GSE233765 | GEO
Project description:Seedling hypocotyls display negative gravitropism in the dark but agravitropism in the light. The Arabidopsis thaliana pif quadruple mutant (pifQ), which lacks four PHYTOCHROME-INTERACTING FACTORS (PIFs), is agravitropic in the dark. Endodermis-specific expression of PIF1 rescues gravitropism in pifQ mutant seedlings. Since phytochromes induce light responses by inhibiting PIFs and the COP1-SPA ubiquitin E3 ligase complex in the nucleus, we asked whether phyB can cell autonomously inhibit hypocotyl negative gravitropism in the endodermis. We found that while epidermis-specific expression of PHYB rescues hypocotyl negative gravitropism and all other phyB mutant phenotypes, endodermis-specific expression of PHYB does not. Epidermal phyB induces the phosphorylation and degradation of endodermal PIFs in response to red light. This induces a global gene expression pattern similar to that induced by red light treatment of seedlings expressing PHYB under the control of its own endogenous promoter. Our results imply that epidermal phyB generates an unidentified mobile signal that travels to the endodermis where it promotes PIF degradation and inhibits hypocotyl negative gravitropism.
2017-02-08 | GSE87591 | GEO
Project description:Phytochrome B-SPA-COP1 regulation of red light induced gene expressions in Arabidopsis thaliana
| PRJNA481068 | ENA
Project description:Background: Photomorphogenesis is repressed in the dark mainly by an E3 ubiquitin ligase complex comprising CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) and four homologous proteins called SUPPRESSOR OF PHYA-105 (SPA1-SPA4) in Arabidopsis. This complex induces the ubiquitination and subsequent degradation of positively acting transcription factors (e.g., HY5, HFR1, PAP1 and others) in the dark to repress photomorphogenesis. Genomic evidence showed a large number of genes regulated by COP1 in the dark, of which many are direct targets of HY5. However, the genomic bases for the constitutive photomorphogenic phenotypes of spaQ remain unknown. Results: Here, we show that >7200 genes are differentially expressed in the spaQ background compared to wild type in the dark. Comparison of the RNAseq data between cop1 and spaQ revealed a large overlapping set of genes regulated by the COP1-SPA complex. In addition, many of the genes coordinately regulated by the COP1-SPA complex are also regulated by HY5 directly and indirectly. Moreover, a large number of genes (~2790) are predominantly regulated by SPA proteins and not by COP1, suggesting that SPA proteins might regulate many biological processes independently of COP1. Conclusions: Taken together, our data reveal that SPA proteins repress photomorphogenesis by controlling expression of a large number of genes in concert with COP1, likely through regulating the abundance of downstream transcription factors in light signaling pathways. Moreover, SPA proteins may function both in a COP1-dependent and –independent manner in regulating many biological processes and developmental pathways in Arabidopsis.
2018-11-05 | GSE112662 | 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:ChIP-seq was performed to map the association of SPA-tagged DnaA across the Escherichia coli MG1655 chromosome during exponential phase growth in LB. As a control to remove background, ChIP-Seq was also performed on SPA-tagged AcpS, a protein that is not known to bind DNA.
2022-10-16 | E-MTAB-12223 | biostudies-arrayexpress
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: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: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