Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA114931 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We compared the transcriptomic response to UVC radiation in widltype (N2), DNA repair-deficient (xpa-1), and germ cell-deficient (glp-1) young adult nematodes. We were interested in the wildtype response to this stressor, and postulated that the early (3h post-exposure) difference might be different in nucleotide excision repair-deficient (xpa-1) nematodes. We also hypothesized that the response would be different in young adults composed entirely of somatic cells (glp-1 strain at this temperature), compared to germ cell-bearing and gravid young adults (N2 and xpa-1). Finally, we compared constitutive differences in gene expression between the strains.
2009-10-19 | GSE15159 | GEO
Project description:Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). We exposed age-matched L1-stage Caenorhabditis elegans to ultraviolet C radiation (UVC ) three times, separated in time by 24 h, in the absence of food. After the third exposure, larvae were placed on K agar plates with OP50 bacterial food. In some cases ethidium bromide was also used. Nematodes were sampled for RNA isolation several times.
2012-10-01 | E-GEOD-38997 | biostudies-arrayexpress
Project description:Spirosoma montaniterrae DY10T is an uncharacterized radiation-resistanct bacteria isolated from soil in South Korea. In order to identify the underlying mechanisms involved in UVC-resistance, we generated time-series transcriptome data with UVC radiation and analyzed data with computational methods.
2023-01-31 | GSE223604 | GEO
Project description:DNA damage caused by UV radiation initiates cellular recovery mechanisms, which involve activation of DNA damage response pathways, cell cycle arrest and apoptosis. To assess cellular transcriptional responses to UVC-induced DNA damage we compared time course responses of human skin fibroblasts to low and high doses of UVC radiation known to induce a transient cellular replicative arrest or apoptosis, respectively. UVC radiation elicited >3-fold changes in 460 out of 12,000 transcripts and 89% of these represented downregulated transcripts. Only 5% of the regulated genes were common to both low and high doses of radiation. Cells inflicted with a low dose of UVC exhibited transcription profiles demonstrating transient regulation followed by recovery, whereas the responses were persistent after the high dose. A detailed clustering analysis and functional classification of the targets implied regulation of biologically divergent responses and suggested involvement of transcriptional and translational machinery, inflammatory, anti-proliferative and anti-angiogenic responses. The data support the notion that UVC radiation induces prominent, dose-dependent downregulation of transcription. However, the data strongly suggest that transcriptional repression is also target gene selective. Furthermore, the results demonstrate that dose-dependent induction of cell cycle arrest and apoptosis by UVC radiation are transcriptionally highly distinct responses. Keywords: other
2003-10-08 | GSE713 | GEO
Project description:Untreated or 20 J/m2 UVC treated RKO cells were collected and RNA from either whole-cell lysates or from polysomal fractions was extracted at 0 (untreated), 3, 6, and 12 h after treatment. RNA from whole-cell lysates or each of 11 polysomal fraction was reverse-transcribed in the presence of [α-33P]dCTP and the radiolabeled product used to hybridize human cDNA arrays. The experiment was repeated using three independent sample sets. The samples were named T-c-A, T-c-B, T-c-C, T-3h-A, T-3h-B, T-3h-C, T-6h-A, T-6h-B, T-6h-C, T-12h-A, T-12h-B, T-12h-C, P-c-1-A, P-c-2-A, P-c-3-A, P-c-4-A, P-c-5-A, P-c-6-A, P-c-7-A, P-c-8-A, P-c-9-A, P-c-10-A, P-c-11-A, P-c-1-B, P-c-2-B, P-c-3-B, P-c-4-B, P-c-5-B, P-c-6-B, P-c-7-B, P-c-8-B, P-c-9-B, P-c-10-B, P-c-11-B, P-c-2-C, P-c-3-C, P-c-4-C, P-c-5-C, P-c-6-C, P-c-7-C, P-c-8-C, P-c-9-C, P-c-10-C, P-c-11-C, P-3h-1-A, P-3h-2-A, P-3h-3-A, P-3h-4-A, P-3h-5-A, P-3h-6-A, P-3h-7-A, P-3h-8-A, P-3h-9-A, P-3h-10-A, P-3h-11-A, P-3h-1-B, P-3h-2-B, P-3h-3-B, P-3h-4-B, P-3h-5-B, P-3h-6-B, P-3h-7-B, P-3h-8-B, P-3h-9-B, P-3h-10-B, P-3h-11-B, P-3h-1-C, P-3h-2-C, P-3h-3-C, P-3h-4-C, P-3h-6-C, P-3h-7-C, P-3h-8-C, P-3h-9-C, P-3h-10-C, P-3h-11-C, P-6h-1-A, P-6h-2-A, P-6h-3-A, P-6h-4-A, P-6h-5-A, P-6h-6-A, P-6h-7-A, P-6h-8-A, P-6h-9-A, P-6h-10-A, P-6h-11-A, P-6h-1-B, P-6h-2-B, P-6h-3-B, P-6h-4-B, P-6h-5-B, P-6h-6-B, P-6h-7-B, P-6h-8-B, P-6h-9-B, P-6h-10-B, P-6h-11-B, P-6h-1-C, P-6h-2-C, P-6h-3-C, P-6h-4-C, P-6h-5-C, P-6h-6-C, P-6h-7-C, P-6h-8-C, P-6h-9-C, P-6h-10-C, P-6h-11-C, P-12h-1-A, P-12h-2-A, P-12h-3-A, P-12h-4-A, P-12h-5-A, P-12h-6-A, P-12h-7-A, P-12h-8-A, P-12h-9-A, P-12h-10-A, P-12h-11-A, P-12h-1-B, P-12h-2-B, P-12h-3-B, P-12h-4-B, P-12h-5-B, P-12h-6-B, P-12h-7-B, P-12h-8-B, P-12h-9-B, P-12h-10-B, P-12h-11-B, P-12h-1-C, P-12h-2-C, P-12h-3-C, P-12h-6-C, P-12h-7-C, P-12h-8-C, P-12h-9-C, P-12h-10-C, P-12h-11-C. ‘T’ represents total RNA, ‘P’ represents RNA from polysomes fractions, ‘c’ represents RNA from untreated cells, ‘3h’ represents RNA from cells collected 3 h after UVC treatment, ‘6h’ represents RNA from cells collected 6 h after UVC treatment, ‘12h’ represents RNA from cells collected 12 h after UVC treatment. The numbers 1-11 correspond to the each polysomal fraction. The letters A, B and C correspond to the three independent experimental datasets. Keywords = post-transcriptional / translation / nascent protein synthesis / stress response / ribonomics Keywords: ordered
2004-06-02 | GSE1440 | GEO
Project description:DNA damage caused by UV radiation initiates cellular recovery mechanisms, which involve activation of DNA damage response pathways, cell cycle arrest and apoptosis. To assess cellular transcriptional responses to UVC-induced DNA damage we compared time course responses of human skin fibroblasts to low and high doses of UVC radiation known to induce a transient cellular replicative arrest or apoptosis, respectively. UVC radiation elicited >3-fold changes in 460 out of 12,000 transcripts and 89% of these represented downregulated transcripts. Only 5% of the regulated genes were common to both low and high doses of radiation. Cells inflicted with a low dose of UVC exhibited transcription profiles demonstrating transient regulation followed by recovery, whereas the responses were persistent after the high dose. A detailed clustering analysis and functional classification of the targets implied regulation of biologically divergent responses and suggested involvement of transcriptional and translational machinery, inflammatory, anti-proliferative and anti-angiogenic responses. The data support the notion that UVC radiation induces prominent, dose-dependent downregulation of transcription. However, the data strongly suggest that transcriptional repression is also target gene selective. Furthermore, the results demonstrate that dose-dependent induction of cell cycle arrest and apoptosis by UVC radiation are transcriptionally highly distinct responses.
2007-09-21 | E-GEOD-713 | biostudies-arrayexpress
Project description:UV-induced CPDs were mapped in isolated human genomic DNA following 80J/m2 of UVC irradiation
2021-08-27 | GSE162125 | GEO
Project description:UV-induced 6-4PPs were mapped in normal human skin fibroblasts following 500J/m2 of UVC irradiation
2021-08-27 | GSE175590 | GEO
Project description:Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair).
2012-10-01 | GSE38997 | GEO
Project description:Untreated or 20 J/m2 UVC treated RKO cells were collected and RNA from either whole-cell lysates or from polysomal fractions was extracted at 0 (untreated), 3, 6, and 12 h after treatment. RNA from whole-cell lysates or each of 11 polysomal fraction was reverse-transcribed in the presence of [α-33P]dCTP and the radiolabeled product used to hybridize human cDNA arrays. The experiment was repeated using three independent sample sets. The samples were named T-c-A, T-c-B, T-c-C, T-3h-A, T-3h-B, T-3h-C, T-6h-A, T-6h-B, T-6h-C, T-12h-A, T-12h-B, T-12h-C, P-c-1-A, P-c-2-A, P-c-3-A, P-c-4-A, P-c-5-A, P-c-6-A, P-c-7-A, P-c-8-A, P-c-9-A, P-c-10-A, P-c-11-A, P-c-1-B, P-c-2-B, P-c-3-B, P-c-4-B, P-c-5-B, P-c-6-B, P-c-7-B, P-c-8-B, P-c-9-B, P-c-10-B, P-c-11-B, P-c-2-C, P-c-3-C, P-c-4-C, P-c-5-C, P-c-6-C, P-c-7-C, P-c-8-C, P-c-9-C, P-c-10-C, P-c-11-C, P-3h-1-A, P-3h-2-A, P-3h-3-A, P-3h-4-A, P-3h-5-A, P-3h-6-A, P-3h-7-A, P-3h-8-A, P-3h-9-A, P-3h-10-A, P-3h-11-A, P-3h-1-B, P-3h-2-B, P-3h-3-B, P-3h-4-B, P-3h-5-B, P-3h-6-B, P-3h-7-B, P-3h-8-B, P-3h-9-B, P-3h-10-B, P-3h-11-B, P-3h-1-C, P-3h-2-C, P-3h-3-C, P-3h-4-C, P-3h-6-C, P-3h-7-C, P-3h-8-C, P-3h-9-C, P-3h-10-C, P-3h-11-C, P-6h-1-A, P-6h-2-A, P-6h-3-A, P-6h-4-A, P-6h-5-A, P-6h-6-A, P-6h-7-A, P-6h-8-A, P-6h-9-A, P-6h-10-A, P-6h-11-A, P-6h-1-B, P-6h-2-B, P-6h-3-B, P-6h-4-B, P-6h-5-B, P-6h-6-B, P-6h-7-B, P-6h-8-B, P-6h-9-B, P-6h-10-B, P-6h-11-B, P-6h-1-C, P-6h-2-C, P-6h-3-C, P-6h-4-C, P-6h-5-C, P-6h-6-C, P-6h-7-C, P-6h-8-C, P-6h-9-C, P-6h-10-C, P-6h-11-C, P-12h-1-A, P-12h-2-A, P-12h-3-A, P-12h-4-A, P-12h-5-A, P-12h-6-A, P-12h-7-A, P-12h-8-A, P-12h-9-A, P-12h-10-A, P-12h-11-A, P-12h-1-B, P-12h-2-B, P-12h-3-B, P-12h-4-B, P-12h-5-B, P-12h-6-B, P-12h-7-B, P-12h-8-B, P-12h-9-B, P-12h-10-B, P-12h-11-B, P-12h-1-C, P-12h-2-C, P-12h-3-C, P-12h-6-C, P-12h-7-C, P-12h-8-C, P-12h-9-C, P-12h-10-C, P-12h-11-C. âTâ represents total RNA, âPâ represents RNA from polysomes fractions, âcâ represents RNA from untreated cells, â3hâ represents RNA from cells collected 3 h after UVC treatment, â6hâ represents RNA from cells collected 6 h after UVC treatment, â12hâ represents RNA from cells collected 12 h after UVC treatment. The numbers 1-11 correspond to the each polysomal fraction. The letters A, B and C correspond to the three independent experimental datasets. Keywords = post-transcriptional / translation / nascent protein synthesis / stress response / ribonomics Keywords: ordered
2010-06-09 | E-GEOD-1440 | biostudies-arrayexpress