Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional effects of TDP1 deficiency in non-replicating U2OS cells

ABSTRACT: Transcriptional effects of TDP1 deficiency in non-replicating U2OS cells

PROVIDER: PRJNA775084 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16597287_1.fastq.gz	Fastqsanger.gz
	SRR16597287_2.fastq.gz	Fastqsanger.gz
	SRR16597288_1.fastq.gz	Fastqsanger.gz
	SRR16597288_2.fastq.gz	Fastqsanger.gz
	SRR16597289_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Transcriptional effects of TDP1 deficiency in non-replicating U2OS cells

Project description:Spinocerebellar ataxia with axonal neuropathy (SCAN1) is a rare recessive neurodegenerative syndrome associated with cerebellar atrophy and peripheral neuropathy. It is caused by a homozygous missense mutation in the tyrosyl-DNA phosphodiesterase-1 (TDP1) gene (A1478G). resulting in a substitution of histidine for arginine-493 (H493R) in the TDP1 catalytic site, leading to reduced TDP1 activity. How TDP1 H493R mutation promotes the SCAN1 phenotype, which is associated with the death of post-mitotic neurons, is unclear. We have generated models of osteosarcoma U2OS cells homozygous for TDP1 H493R employing the CRISPR-Cas9 technique (2 clones, named “1P” and “3.3”). Here, we have generated transcriptional genome wide profile in order to characterize differences in gene expression that are specific of TDP1-mutated clones.

2024-04-30 | GSE186693 | GEO

TDP1 gene knockout effect on transcriptome

Project description:TDP1 is an enzyme that in humans is encoded by the TDP1 gene.[5][6][7] TDP1 is the protein involved in repairing stalled topoisomerase I-DNA complexes. We evaluated the effect of Tdp1 knockout in HEK293A cells on the gene expression.

2023-11-20 | GSE247361 | GEO

Investigation of genetic compensation in tdp1-/- zebrafish embryos

Project description:Tdp1, tyrosyl-DNA phosphodiesterase 1, is an enzyme responsible for the repair of DNA breaks resulting from aberrant topoisomerase 1 activity, called Top1 cleavage complexes (Top1-CCs). Mutation of Tdp1 leads to a progressive neurodegenerative disorder spinocerebellar ataxia with axonal neuropathy 1 (SCAN1). We have generated tdp1-/- zebrafish as a model for SCAN1. The adult fish have a behavioral defect and hypersensitivity to camptothecin (CPT), a Top1 poison. Strikingly, the embryos do not show increased sensitivity to CPT, unlike any other reported vertebrate models, suggesting genetic compensation is at play at this stage. We thus carried out microarray analysis in CPT-treated zebrafish embryos to compare the gene expression profiles of tdp1WT and tdp1-/- genotypes. Gene expression analysis revealed 1,8111 genes that were differentially expressed: 1,071 were upregulated and 740 were downregulated. Sprtn and neil1, two potential compensation candidates were upregulated in the tdp1-/- embryos.

2022-04-19 | GSE148923 | GEO

TDP1 mutation causing SCAN1 neurodegenerative syndrome hampers the repair of transcriptional DNA double-strand breaks

Project description:TDP1 removes transcription-blocking TOP1 cleavage complexes (TOP1ccs) and its inactivating H493R mutation causes the neurodegenerative syndrome SCAN1. However, the molecular mechanism underlying SCAN1 phenotype is unclear. Here, we generate human SCAN1 cell models using CRISPR/Cas9 and show that they accumulate TOP1ccs along with changes in gene expression and genomic distribution of R-loops. SCAN1 cells also accumulate transcriptional DNA double-strand breaks (DSBs) specifically in the G1 cell population due to increased DSB formation and lack of repair, both resulting from abortive removal of transcription-blocking TOP1ccs. Deficient TDP1 activity causes increased DSB production and the presence of mutated TDP1 protein hampers DSB repair by a TDP2-dependent back-up pathway. This study provides powerful models to study TDP1 functions under physiological and pathological conditions and unravels that a gain of function of the mutated TDP1 protein, which prevents DSB repair, rather than a loss of TDP1 activity itself, could contribute to SCAN1 pathogenesis.

2024-04-25 | GSE226263 | GEO

Extracellular vesicles secreted from HBV-replicating or non-replicating cells

Project description:LC/MS proteomic analysis of EVs secreted from HBV-replicating or non-replicating cells was performed.

2020-08-14 | PXD018292 | JPOST Repository

U2OS-ERa, U2OS-ERb, and U2OS-ERab cells treated with 4HT or E2

Project description:U2OS-ERa, U2OS-ERb, and U2OS-ERab cells treated with 4HT or E2 Keywords: other

2005-04-06 | GSE2292 | GEO

Whole-genome CRISPR screen of etoposide-treated U2OS and U2OS p53KO cells, and RNAseq of U2OS cells incubated in media conditioned by etoposide-treated U2OS or U2OS p53KO cells.

Project description:CRISPR screen: U2OS or U2OS p53KO cells expressing Cas9 were transduced with a whole-genome library of CRISPR sgRNAs, then treated with either DMSO or etoposide. Differential sgRNA abundances were calculated for each condition and used to determine the effect of each single gene knockout on fitness and the drug-induced death rate. RNA-Seq: U2OS or U2OS p53KO cells were cultured with either DMSO or etoposide for 48 hours, and then U2OS cells were incubated in this conditioned media for 8 hours. RNA was collected and use to observe differential expression changes between conditions.

2023-05-17 | GSE232592 | GEO

TDP1 gene knockout effect on transcriptome

Project description:TDP1 gene knockout effect on transcriptome

| PRJNA1037162 | ENA

TDP1 phosphorylation at S61 promotes Top1cc repair via the MUS81-dependent pathway during mitosis

Project description:Topoisomerase 1 (Top1) removes supercoils from DNA during replication and transcription, is critical for mitotic progression to the G1 phase, and ensures DNA topology. Tyrosyl-DNA phosphodiesterase 1 (TDP1) mediates the removal of trapped Top1-DNA covalent complexes (Top1ccs). Here, we identify CDK1-dependent phosphorylation of TDP1 at S61 residue during mitosis. TDP1 defective for S61 phosphorylation (TDP1S61A) is trapped on the mitotic chromosomes, triggering DNA damage and mitotic defects. Moreover, we show that Top1cc repair in mitosis occurs via MUS81-dependent mitotic DNA repair mechanism. Replication stress (RS) induced by Camptothecin (CPT) or Aphidicolin (APH) leads to TDP1S61A enrichment at common fragile sites (CFSs), which over-stimulates MUS81-dependent chromatid breaks, anaphase bridges, and micronuclei, ultimately culminating in 53BP1 nuclear bodies in the G1-phase. Our findings provide a new insight into the cell cycle-dependent regulation of TDP1 dynamics forthe repair of trapped Top1ccs during mitosis that prevents genomic instability following RS.

2024-06-26 | PXD053309 | Pride

Non-circadian expression masking clock-driven weak transcription rhythms in U2OS cells

Project description:U2OS cells harbor a circadian clock but express only a few rhythmic genes in constant conditions. We identified 3040 binding sites of the circadian regulators BMAL1, CLOCK and CRY1 in the U2OS genome. Most binding sites even in promoters do not correlate with detectable rhythmic transcript levels. Luciferase fusions reveal that the circadian clock supports robust but low amplitude transcription rhythms of representative promoters. However, rhythmic transcription of these potentially clock-controlled genes is masked by non-circadian transcription that overwrites the weaker contribution of the clock in constant conditions. Our data suggest that U2OS cells harbor an intrinsically rather weak circadian oscillator. The oscillator has the potential to regulate a large number of genes. The contribution of circadian versus non-circadian transcription is dependent on the metabolic state of the cell and may determine the apparent complexity of the circadian transcriptome. Analysis of temporal expression profiles of 5708 expressed genes in synchronized U2OS cells.

2014-05-23 | GSE57891 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data