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Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging

ABSTRACT: Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging

PROVIDER: PRJNA550140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9417430.fastq.gz	Fastqsanger.gz
	SRR9417440.fastq.gz	Fastqsanger.gz
	SRR9417431.fastq.gz	Fastqsanger.gz
	SRR9417441.fastq.gz	Fastqsanger.gz
	SRR9417432.fastq.gz	Fastqsanger.gz

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Similar Datasets

Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging

Project description:Cockayne syndrome (CS) is an accelerated aging disorder, caused by mutations in the CSA or CSB genes. In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and PARP consumes and depletes cellular nicotinamide adenine dinucleotide (NAD), which leads to mitochondrial dysfunction. Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the results show striking enrichment of PAR at transcription start sites (TSS), depletion of heterochromatin, and downregulation of H3K9me3-specific methyltransferases SUV39H1 and SETDB1. Induced-expression of SETDB1 in CSB-deficient cells downregulated PAR and normalized mitochondrial function. The results suggest that defects in CSB are strongly associated with loss of heterochromatin, downregulation of SETDB1, increased PAR in highly-transcribed regions, and mitochondrial dysfunction.

2019-06-22 | GSE133176 | GEO

Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging.

Project description:Cockayne syndrome is an accelerated aging disorder, caused by mutations in the CSA or CSB genes. In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitochondrial dysfunction. Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the results show striking enrichment of PAR at transcription start sites, depletion of heterochromatin and downregulation of H3K9me3-specific methyltransferases SUV39H1 and SETDB1. Induced-expression of SETDB1 in CSB-deficient cells downregulated PAR and normalized mitochondrial function. The results suggest that defects in CSB are strongly associated with loss of heterochromatin, downregulation of SETDB1, increased PAR in highly-transcribed regions, and mitochondrial dysfunction.

| S-EPMC6895253 | biostudies-literature

Setdb1 is required for persistence of H3K9me3 and repression of endogenous retroviruses in mouse primordial germ cells

Project description:Transcription of endogenous retroviruses (ERVs) is inhibited by de novo DNA methylation during gametogenesis, a process initiated after birth in oocytes and at ~E15.5 in prospermatogonia. Earlier in germline development however, the genome, including most retrotransposons, is progressively demethylated, with young ERVK and ERV1 elements retaining intermediate methylation levels. As DNA methylation reaches a low point in E13.5 primordial germ cells (PGCs) of both sexes, we determined whether retrotransposons are marked by H3K9me3 and H3K27me3 using a recently developed low input ChIP-seq method. Although these repressive histone modifications are predominantly found on distinct genomic regions in E13.5 PGCs, they concurrently mark partially methylated LTRs and LINE1 elements. Germline-specific conditional knock-out (KO) of the H3K9 methyltransferase SETDB1 yields a decrease of both histone marks and DNA methylation at H3K9me3 enriched retrotransposon families. Strikingly, Setdb1-KO E13.5 PGCs show concomitant de-repression of many marked ERVs, including IAP, ETn and ERVK10C elements and ERV-proximal genes, a subset in a sex-dependent manner. Furthermore, Setdb1 deficiency is associated with a reduced number of male PGCs and postnatal hypogonadism in both sexes. Taken together, these observations reveal that SETDB1 is an essential guardian against proviral expression prior to the onset of de novo DNA methylation in the germline. H3K9me3, H3K27me3 and expression profiles in Setdb1 WT, Het and KO male and female E13.5 PGCs.

2014-09-01 | E-GEOD-60377 | biostudies-arrayexpress

Next Generation Sequencing to Facilitate Quantitative Analysis of wild type, setdb1 GLKD and snf[148] ovary H3K9me3 binding profiles [ChIP-seq]

Project description:Comparison of wild type, setdb1 GLKD, and snf[148] H3K9me3 profiles shows that SXL facilitates H3K9me3 deposition on SETDB1 regulated genes

2018-09-07 | GSE109851 | GEO

Identification of Setdb1 interaction proteins in neural stem cells

Project description:Setdb1 is an epigenetic factors catalyzing modification of H3K9me3. Expression of its gene is localized to embryonic neural cells during vertebrate embryogenesis, suggesting its role in regulating neural stemness. The project is to identify the interaction partners of Setdb1, by which Setdb1 regulates neural stemness in neural stem cells.

2022-08-12 | PXD030453 | Pride

Setdb1 regulates Cohesin at H3K9me3-independent topological domains

Project description:Setdb1 regulates Cohesin at H3K9me3-independent topological domains

| PRJNA507948 | ENA

H3K9me3 ChIP-seq in HeLa cells lacking TASOR, MPP8, periphilin and SETDB1

Project description:We performed ChIP-seq to measure H3K9me3 levels in wild-type HeLa cells and HeLa cells lacking TASOR, MPP8, periphilin and SETDB1 generated through CRISPR/Cas9-mediated gene disruption.

2015-05-28 | GSE63116 | GEO

DNA methylation and SETDB1/H3K9me3 regulate predominantly distinct sets of genes, retroelements and chimaeric transcripts in mouse ES cells

Project description:DNA methylation and histone H3 lysine 9 trimethylation (H3K9me3) play important roles in silencing of genes and retroelements. However, a comprehensive comparison of genes and repetitive elements repressed by these pathways has not been reported. Here we show that in mouse embryonic stem cells (mESCs), the genes up-regulated following deletion of the H3K9 methyltransferase Setdb1 are distinct from those de-repressed in mESC deficient in the DNA methyltransferases Dnmt1, Dnmt3a and Dnmt3b, with the exception of a small number of primarily germline-specific genes. Numerous endogenous retroviruses (ERVs) lose H3K9me3 and are concomitantly de-repressed exclusively in SETDB1 knockout mESCs. Strikingly, ~15% of up-regulated genes are induced in association with de-repression of promoter proximal ERVs, half in the context of "chimaeric" transcripts that initiate within these retroelements and splice to genic exons. Thus, SETDB1 plays a previously unappreciated yet critical role in inhibiting aberrant gene transcription by suppressing the expression of proximal ERVs. NChIP-seq and mRNA-seq of WT, SETDB1 KO and DMNT1 TKO mESCs

2011-05-21 | E-GEOD-29413 | biostudies-arrayexpress

ChIP-Seq of chromatin remodeler SMARCAD1 and H3K9me3 in female mouse embryonic stem cells (PGK12.1 XX)

Project description:Investigation of the co-occurance of the ATP-dependent chromatin remodeler SMARCAD1 and the histone modification H3K9me3 in the genome of PGK12.1 XX ES cells. ChIP-seq of endogenous SMARCAD1 was carried out in control and SMARCAD1-knockdown ES cells using a double crosslinking procedure. Additionally, H3K9me3 ChIP-seq was performed in double-cross linked control PGK12.1 XX cells. Input samples and precipitates with an IgG antibody were sequenced (Illumina HiSeq1500) as controls. Antibodies used were SMARCAD1 PAB15737 (Abnova) and H3K9me3 ab8898 (abcam).

2019-02-17 | E-MTAB-7012 | biostudies-arrayexpress

H3K9me3 chIP-seq 5 days following disruption of the SETDB1 H3K9 trimethylase with two different sgRNAs (6, and 9) or non-targeting control

Project description:We performed H3K9me3 chIP-seq 5 days following disruption of the SETDB1 H3K9 trimethylase with two different sgRNAs (6, and 9) or non-targeting control. Our data suggests that H3K9me3 is modestly reduced over transposable elements and some ZNF genes following disruption of SETDB1.

2017-09-06 | GSE103408 | GEO

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