Regulation of plant DNA methylation by UV-B light in Arabidopsis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA549508 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13194200.fastq.gz | Fastqsanger.gz | |||
| SRR13194201.fastq.gz | Fastqsanger.gz | |||
| SRR13194202.fastq.gz | Fastqsanger.gz | |||
| SRR13194203.fastq.gz | Fastqsanger.gz | |||
| SRR13194204.fastq.gz | Fastqsanger.gz |
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Project description:This study investigated the effect of UV-B treatment on DNA methylation in A. thaliana.
2020-12-04 | GSE132944 | GEO
Project description:Ouyang2014 - photomorphogenic UV-B signalling
network
This model is described in the article:
Coordinated photomorphogenic
UV-B signaling network captured by mathematical modeling.
Ouyang X, Huang X, Jin X, Chen Z,
Yang P, Ge H, Li S, Deng XW.
Proc. Natl. Acad. Sci. U.S.A. 2014 Aug;
111(31): 11539-11544
Abstract:
Long-wavelength and low-fluence UV-B light is an
informational signal known to induce photomorphogenic
development in plants. Using the model plant Arabidopsis
thaliana, a variety of factors involved in UV-B-specific
signaling have been experimentally characterized over the past
decade, including the UV-B light receptor UV resistance locus
8; the positive regulators constitutive photomorphogenesis 1
and elongated hypocotyl 5; and the negative regulators cullin4,
repressor of UV-B photomorphogenesis 1 (RUP1), and RUP2.
Individual genetic and molecular studies have revealed that
these proteins function in either positive or negative
regulatory capacities for the sufficient and balanced
transduction of photomorphogenic UV-B signal. Less is known,
however, regarding how these signaling events are
systematically linked. In our study, we use a systems biology
approach to investigate the dynamic behaviors and correlations
of multiple signaling components involved in Arabidopsis
UV-B-induced photomorphogenesis. We define a mathematical
representation of photomorphogenic UV-B signaling at a temporal
scale. Supplemented with experimental validation, our
computational modeling demonstrates the functional interaction
that occurs among different protein complexes in early and
prolonged response to photomorphogenic UV-B.
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2024-09-02 | BIOMD0000000545 | BioModels
Project description:LAP-35 and SK-N_MC cells were treated with 10 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with SK-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in SK-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in SK-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of SK-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in SK-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression.
2015-10-20 | GSE59889 | GEO
Project description:Ultraviolet (UV) light induces the formation of bulky UV photoproducts in the genome that interfere with DNA replication and transcription. It is well-established how human cells repair UV light-induced DNA lesions, however the signaling pathways and mechanisms that regulate transcription after exposure to UV light are poorly understood. Here, we provide a systematic view on dynamic protein phosphorylation patterns induced by UV light and uncover the dependencies of phosphorylation events on canonical DNA damage kinases and the p38 MAP kinase pathway. Notably, we demonstrate that p38 and its downstream effector kinase MK2 are responsible for one quarter of protein phosphorylation induced by UV light. We identify RNA binding proteins as primary targets and 14-3-3 family proteins as direct readers of UV light-induced, p38-MK2-dependent phosphorylation. Importantly, we demonstrate that UV light triggers rapid and dynamic phosphorylation of the negative elongation factor (NELF) complex subunit NELFE on serine 115 that mediates its binding to 14-3-3. NELFE interaction with 14-3-3 stabilizes NELFE and RNA pol II interaction on the chromatin and inhibits transcriptional elongation, thereby promoting cell survival after UV light.
2019-11-24 | GSE90555 | GEO
Project description:Ultraviolet (UV) light induces the formation of bulky UV photoproducts in the genome that interfere with DNA replication and transcription. It is well-established how human cells repair UV light-induced DNA lesions, however the signaling pathways and mechanisms that regulate transcription after exposure to UV light are poorly understood. Here, we provide a systematic view on dynamic protein phosphorylation patterns induced by UV light and uncover the dependencies of phosphorylation events on canonical DNA damage kinases and the p38 MAP kinase pathway. Notably, we demonstrate that p38 and its downstream effector kinase MK2 are responsible for one quarter of protein phosphorylation induced by UV light. We identify RNA binding proteins as primary targets and 14-3-3 family proteins as direct readers of UV light-induced, p38-MK2-dependent phosphorylation. Importantly, we demonstrate that UV light triggers rapid and dynamic phosphorylation of the negative elongation factor (NELF) complex subunit NELFE on serine 115 that mediates its binding to 14-3-3. NELFE interaction with 14-3-3 stabilizes NELFE and RNA pol II interaction on the chromatin and inhibits transcriptional elongation, thereby promoting cell survival after UV light.
2019-11-24 | GSE90554 | GEO
Project description:human hepatoma Hep3B cells were treated with 10 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with Hep3B_UV_40J-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in Hep3B_UV_40J-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in Hep3B_UV_40J-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of Hep3B_UV_40J-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in Hep3B_UV_40J-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression.
2015-10-20 | GSE65678 | GEO
Project description:human hepatoma Hep3B cells were treated with 40 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with Hep3B_UV_40J-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in Hep3B_UV_40J-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in Hep3B_UV_40J-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of Hep3B_UV_40J-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in Hep3B_UV_40J-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression.
2015-02-06 | GSE65676 | GEO
Project description:LAP-35 and SK-N_MC cells were treated with 10 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with SK-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in SK-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in SK-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of SK-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in SK-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression. Three biological replicates were labeled in direct and dye-swap microarray experiments and hybridized onto an Agilent custom splicing-sensitive microarray platform
2015-10-20 | E-GEOD-59889 | biostudies-arrayexpress
Project description:human hepatoma Hep3B cells were treated with 40 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with Hep3B_UV_40J-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in Hep3B_UV_40J-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in Hep3B_UV_40J-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of Hep3B_UV_40J-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in Hep3B_UV_40J-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression. Three biological replicates were labeled in direct and dye-swap microarray experiments and hybridized onto an Agilent custom splicing-sensitive microarray platform
2015-02-06 | E-GEOD-65676 | biostudies-arrayexpress
Project description:UV-B (280-320 nm) exposure causes serious damage in plants, limiting their growth and survival, effects that are partly counteracted by repair mechanisms active in plants receiving accompanying visible radiation. Though no particular UV-B receptor has been identified to date, there is strong evidence to indicate that certain aspects of UV-B perception are receptor-mediated. Investigations of down-stream signalling events have thus far indicated broad similarities to pathogen-induced defence responses in plants. In order to identify genes in Arabidopsis that may be up- or down- regulated specifically in response to UV-B exposure and compare them to genes whose expression is altered in plants challenged by an avirulent isolate of Peronospora parasitica (downy mildew), we propose to analyse the transcriptional profiles for the following treatments: 1. UV-B Responses "A-1" Columbia (Col-0) exposed to supplementary UV-B/UV-A* with a background of low photosynthetically active radiation (PAR of 20 micromol m-2 s-1) for 1.5 photoperiods (photoperiod = 12h). [UV-B treatment] "A-2" Col-0 exposed to supplementary UV-A and low PAR for 1.5 photoperiods [control for UV-B treatment] "A-3" Col-0 exposed to visible light only (low PAR) (no UV) for 1.5 photoperiods [control for UV effects in general].* There are no pure sources of UV-B light available. 2. Pathogen Responses "A-4" Col-0 spray-inoculated with P. parasitica isolate HIKS-1 (recognised by the R-gene RPP7). After spraying, plants were kept covered in plant propagators and transferred to an 18 degreeC growth chamber. !Samples for RNA extraction were taken 72h after inoculation. "A-5" The viability of spores was also checked by parallel spraying of the susceptible mutant, Col-rpp7. [pathogen treatment] "A-6" Col-0 mock treated with water, covered and transferred to an 18 degree C growth chamber, 72h prior to sampling. [control for pathogen treatment] In all experiments, we are using RNA from leaves taken at the same time of day (6 h into the 12 h photoperiod) from 4.5-week old plants grown under 12h photoperiod. All treatments were normalised against PR-1 expression levels to ensure comparability between UV-B and pathogen treatments. Due to the difficulty in distinguishing between local and systemic induced responses in UV-B treated plants, we are using RNA from whole rosettes for both the UV-B and pathogen treatment for better comparability among treatments. The degree of similarity between these two sets of transcriptional changes will complement and help interpret our experimental data on changes in resistance to pathogens in plants pre-treated with UV-B. Moreover, the data set obtained would allow for identification of UV-B specific changes in gene expression including cis-acting UV-B-responsive promoter elements. Experimenter name = Julia Brueggemann Experimenter phone = 01789 470 382 Experimenter fax = 01789 470 552 Experimenter address = Horticulture Research International Experimenter address = Wellesbourne Experimenter address = Warwickshire Experimenter zip/postal_code = CV35 9EF Experimenter country = UK Keywords: stimulus_or_stress_design
2007-01-08 | GSE5731 | GEO