Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Amniotes co-opt intrinsic genetic instability to protect germ-line genome integrity

ABSTRACT: Amniotes co-opt intrinsic genetic instability to protect germ-line genome integrity

PROVIDER: PRJNA694114 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13508736_1.fastq.gz	Fastqsanger.gz
	SRR13508736_2.fastq.gz	Fastqsanger.gz
	SRR13508737_1.fastq.gz	Fastqsanger.gz
	SRR13508737_2.fastq.gz	Fastqsanger.gz
	SRR13508738.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 141

Similar Datasets

Amniotes co-opt intrinsic genetic instability to protect germ-line genome integrity.

Project description:Unlike PIWI-interacting RNA (piRNA) in other species that mostly target transposable elements (TEs), >80% of piRNAs in adult mammalian testes lack obvious targets. However, mammalian piRNA sequences and piRNA-producing loci evolve more rapidly than the rest of the genome for unknown reasons. Here, through comparative studies of chickens, ducks, mice, and humans, as well as long-read nanopore sequencing on diverse chicken breeds, we find that piRNA loci across amniotes experience: (1) a high local mutation rate of structural variations (SVs, mutations ≥ 50 bp in size); (2) positive selection to suppress young and actively mobilizing TEs commencing at the pachytene stage of meiosis during germ cell development; and (3) negative selection to purge deleterious SV hotspots. Our results indicate that genetic instability at pachytene piRNA loci, while producing certain pathogenic SVs, also protects genome integrity against TE mobilization by driving the formation of rapid-evolving piRNA sequences.

| S-EPMC9925758 | biostudies-literature

Amniotes co-opt intrinsic genetic instability to protect germ-line genome integrity

Project description:We applied high-throughput sequencing on rooster testis samples.

2023-01-24 | GSE165330 | GEO

Senataxin associates with replication forks to protect fork integrity across RNAPII transcribed genes

Project description:Here we analysed the role of yeast Senataxin (Sen1) in coordinating replication with transcription and in protecting genome integrity. Senataxin is mutated in the two severe neurodegenerative diseases AOA2 and ALS4. We show that a fraction of Sen1/Senataxin DNA/RNA helicase associates with replication forks and protects the integrity of those fork encountering highly expressed RNAPII genes. sen1 mutants accumulate aberrant DNA structures and RNA-DNA hybrids while forks clash head-on with RNAPII transcription units and counteract recombinogenic events and accumulation of checkpoint signals. Nrd1, which acts togheter with Sen1 in trascription temination, is not recruited at replication forks. nrd1 mutants does not display replication defects, high genome instability and checkpoint activation observed in sen1 mutants The Sen1 function in replication can be therefore separable from its role in RNA processing. We propose a role for Sen1/Senataxin during chromosome replication in facilitating replisome progression across RNAPII transcribed genes thus preventing DNA-RNA hybrids accumulation when forks encounter nascent transcripts on the lagging strand template. Chip on chip analysis was carried out as described (Bermejo et al., 2011), employing anti-Flag monoclonal antibody M2 (Sigma-Aldrich) Labelled probes were hybridized to Affymetrix S.cerevisiae Tiling 1.0 (P/N 900645) arrays and processed with TAS software.

2012-11-09 | E-GEOD-39139 | biostudies-arrayexpress

TGF-β promotes genomic instability after loss of RUNX3

Project description:Studies of genomic instability have historically focused on intrinsic mechanisms rather than extrinsic mechanisms based in the tumor microenvironment (TME). TGF-β is the most abundantly secreted cytokine in the TME where it imparts various aggressive characteristics including invasive migration, drug resistance and epithelial-to-mesenchymal transition (EMT). Here we show that TGF-β also promotes genomic instability in the form of DNA double strand breaks (DSB) in cancer cells which lack the tumor suppressor gene RUNX3. Loss of RUNX3 resulted in transcriptional downregulation of the redox regulator heme oxygenase-1 (HO-1 or HMOX1). Consequently, elevated oxidative DNA damage disrupted genomic integrity and triggered cellular senescence, which was accompanied by tumor-promoting inflammatory cytokine expression and acquisition of the senescence-associated secretory phenotype (SASP). Recapitulating the above findings, tumors harbouring a TGF-β gene expression signature and RUNX3 loss exhibited higher levels of genomic instability. In summary, RUNX3 creates an effective barrier against further TGF-β-dependent tumor progression by preventing genomic instability. These data suggest a novel cooperation between cancer cell-extrinsic TGF-β signaling and cancer cell-intrinsic RUNX3 inactivation as aggravating factors for genomic instability.

2019-06-20 | GSE133037 | GEO

Erwinia sp. OPT-41

Project description:Erwinia sp. OPT-41 Genome sequencing

| PRJNA1137566 | ENA

Senataxin associates with replication forks to protect fork integrity across RNAPII transcribed genes

2012-11-09 | GSE39139 | GEO

Opt-In Versus Opt-Out for Colorectal Cancer Screening Outreach

Project description:This is a randomized controlled pilot study aimed at testing different outreach strategies (opt-in versus opt-out) to increase colorectal cancer screening through completion of mailed home fecal immunohistochemical testing (FIT).

| 2227183 | ecrin-mdr-crc

THC Protect

Project description:Thc protect llc

| PRJNA1097369 | ENA

Mitochondrial integrity regulated by FABP5 is a cell-intrinsic checkpoint for Treg suppressive function

Project description:Mitochondrial integrity regulated by FABP5 is a cell-intrinsic checkpoint for Treg suppressive function

| PRJNA521378 | ENA

Bcl-xL is required to protect endothelial cells latently infected with KSHV from virus induced intrinsic apoptosis

Project description:Bcl-xL is required to protect endothelial cells latently infected with KSHV from virus induced intrinsic apoptosis

| PRJNA942262 | ENA