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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The role of DNA repair endonuclease XPF in transcription

ABSTRACT: In this experiment we want to explore and compare the bindind of XPF in normal MEFs, in tRA treated MEFs and in UV radiated MEFs

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Mus musculus

SUBMITTER: George Garinis

PROVIDER: E-MTAB-8154 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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XAB2 binds genome-wide on putative DNA elements (e.g. enhancers, promoters) that are known to regulate gene expression

Project description:XAB2 ChIP-Seq profile of mESCs treated with trans-retinoic acid (tRA), a pleiotropic factor known to activate transcription and regulate gene expression during cell differentiation and embryonic development and CHIP-Seq profile of the same cells untreated.

2020-08-19 | E-MTAB-8033 | biostudies-arrayexpress

RNA-Seq profiling of ERCC1-XPF DNA repair defect (Er1F/-) versus wild type (Er1F/+) macrophages

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The role of DNA repair endonuclease XPF in transcription

Project description:The role of DNA repair endonuclease XPF in transcription

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RNA-seq of mouse DNA repair endonuclease XPF knock out versus wild type and versus trans retinoic acid (tRA) treated wild type

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P300-mediated adaptive conversion of glioma stem cells to vascular-like cells in response to therapeutic stress promotes tumor recurrence [RNA-seq_sorted GEC GPC]

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Gene expression induced in HEK293 by treatment with the differentiating agents all-trans retinoic acid (tRA) and N6,2'-O-dibutyryl-cAMP (cAMP)

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Expression data from Sotos syndrome patients and controls

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Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.

Project description:We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. Eight mixed stage C. elegans samples were run on Affymetrix GeneChip C. elegans Genome Arrays. Four samples belong to ercc-1 mutant group and four to the wild-type, N2.

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