Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA259337 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1556900_1.fastq.gz | Fastqsanger.gz | |||
| SRR1556900_2.fastq.gz | Fastqsanger.gz | |||
| SRR1556910_1.fastq.gz | Fastqsanger.gz | |||
| SRR1556910_2.fastq.gz | Fastqsanger.gz | |||
| SRR1556920_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 54 |
Similar Datasets
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
Project description:During mammalian development DNA methylation patterns need to be reset in primordial germ cells (PGC) and preimplantation embryos. However, many retro-transposons and imprinted genes are resistant to such global epigenetic reprogramming via hitherto undefined mechanisms. Here, we report that some of these sequences are immune to widespread erasure of DNA methylation in the mouse embryonic stem cells (mESCs) lacking de novo DNA methyltransferases. Persistence of DNA methylation at these loci in mESCs depends on the histone H3K9 methyltransferase Setdb1, as deletion of Setdb1 results in reduction of H3K9me3 and DNA methylation levels concomitant with an increase in 5-hydroxymethylation (5hmC). In addition, depletion of H3K9 methyltransferase G9a leads to genome-wide reduction of DNA methylation but to a lesser extent at the above sequences. Taken together, these data reveal that Setdb1 ensures the fidelity of DNA methylation at specific loci in mESCs, which may reflect mechanisms functioning in vivo during key developmental stages. Examination of H3K9me3 histone modifications in 2 cell types.
2014-06-03 | E-GEOD-47878 | biostudies-arrayexpress
Project description:During mammalian development DNA methylation patterns need to be reset in primordial germ cells (PGC) and preimplantation embryos. However, many retro-transposons and imprinted genes are resistant to such global epigenetic reprogramming via hitherto undefined mechanisms. Here, we report that some of these sequences are immune to widespread erasure of DNA methylation in the mouse embryonic stem cells (mESCs) lacking de novo DNA methyltransferases. Persistence of DNA methylation at these loci in mESCs depends on the histone H3K9 methyltransferase Setdb1, as deletion of Setdb1 results in reduction of H3K9me3 and DNA methylation levels concomitant with an increase in 5-hydroxymethylation (5hmC). In addition, depletion of H3K9 methyltransferase G9a leads to genome-wide reduction of DNA methylation but to a lesser extent at the above sequences. Taken together, these data reveal that Setdb1 ensures the fidelity of DNA methylation at specific loci in mESCs, which may reflect mechanisms functioning in vivo during key developmental stages. Examination of H3K9me3 histone modifications in 2 cell types.
2014-06-03 | E-GEOD-47887 | biostudies-arrayexpress
Project description:Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications, such as H3K9me3 and DNA methylation. Their impact on ERV silencing differs in various cell types and, no systematic analyses on the interdependence between H3K9me3 and DNA methylation have been performed in differentiated cells. Here we show that deletion of the H3K9me3 HMTase Setdb1 in mouse embryonic endoderm results in ERV de-repression in only a subset of endoderm cells. We found that de-repression is restricted to visceral endoderm descendants and does not occur in definitive endoderm cells. Deletion of Setdb1 in visceral endoderm progenitors resulted in loss of H3K9me3 and reduced DNA methylation of IAPEz, consistent with up-regulation of this ERV family. In definitive endoderm cells, loss of Setdb1 did not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 ko resulted in ERV de-repression in both visceral and definitive endoderm cells, while H3K9me3 was unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 in ERV silencing in endoderm cells. Our findings suggest, that H3K9me3 is not sufficient for ERV silencing, but rather critical for maintaining high DNA methylation.
2022-08-01 | GSE139127 | GEO
Project description:Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications, such as H3K9me3 and DNA methylation. Their impact on ERV silencing differs in various cell types and, no systematic analyses on the interdependence between H3K9me3 and DNA methylation have been performed in differentiated cells. Here we show that deletion of the H3K9me3 HMTase Setdb1 in mouse embryonic endoderm results in ERV de-repression in only a subset of endoderm cells. We found that de-repression is restricted to visceral endoderm descendants and does not occur in definitive endoderm cells. Deletion of Setdb1 in visceral endoderm progenitors resulted in loss of H3K9me3 and reduced DNA methylation of IAPEz, consistent with up-regulation of this ERV family. In definitive endoderm cells, loss of Setdb1 did not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 ko resulted in ERV de-repression in both visceral and definitive endoderm cells, while H3K9me3 was unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 in ERV silencing in endoderm cells. Our findings suggest, that H3K9me3 is not sufficient for ERV silencing, but rather critical for maintaining high DNA methylation.
2022-08-01 | GSE169463 | GEO
Project description:Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications, such as H3K9me3 and DNA methylation. Their impact on ERV silencing differs in various cell types and, no systematic analyses on the interdependence between H3K9me3 and DNA methylation have been performed in differentiated cells. Here we show that deletion of the H3K9me3 HMTase Setdb1 in mouse embryonic endoderm results in ERV de-repression in only a subset of endoderm cells. We found that de-repression is restricted to visceral endoderm descendants and does not occur in definitive endoderm cells. Deletion of Setdb1 in visceral endoderm progenitors resulted in loss of H3K9me3 and reduced DNA methylation of IAPEz, consistent with up-regulation of this ERV family. In definitive endoderm cells, loss of Setdb1 did not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 ko resulted in ERV de-repression in both visceral and definitive endoderm cells, while H3K9me3 was unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 in ERV silencing in endoderm cells. Our findings suggest, that H3K9me3 is not sufficient for ERV silencing, but rather critical for maintaining high DNA methylation.
2022-08-01 | GSE169462 | GEO
Project description:Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications, such as H3K9me3 and DNA methylation. Their impact on ERV silencing differs in various cell types and, no systematic analyses on the interdependence between H3K9me3 and DNA methylation have been performed in differentiated cells. Here we show that deletion of the H3K9me3 HMTase Setdb1 in mouse embryonic endoderm results in ERV de-repression in only a subset of endoderm cells. We found that de-repression is restricted to visceral endoderm descendants and does not occur in definitive endoderm cells. Deletion of Setdb1 in visceral endoderm progenitors resulted in loss of H3K9me3 and reduced DNA methylation of IAPEz, consistent with up-regulation of this ERV family. In definitive endoderm cells, loss of Setdb1 did not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 ko resulted in ERV de-repression in both visceral and definitive endoderm cells, while H3K9me3 was unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 in ERV silencing in endoderm cells. Our findings suggest, that H3K9me3 is not sufficient for ERV silencing, but rather critical for maintaining high DNA methylation.
2022-08-01 | GSE139126 | GEO
Project description:Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications, such as H3K9me3 and DNA methylation. Their impact on ERV silencing differs in various cell types and, no systematic analyses on the interdependence between H3K9me3 and DNA methylation have been performed in differentiated cells. Here we show that deletion of the H3K9me3 HMTase Setdb1 in mouse embryonic endoderm results in ERV de-repression in only a subset of endoderm cells. We found that de-repression is restricted to visceral endoderm descendants and does not occur in definitive endoderm cells. Deletion of Setdb1 in visceral endoderm progenitors resulted in loss of H3K9me3 and reduced DNA methylation of IAPEz, consistent with up-regulation of this ERV family. In definitive endoderm cells, loss of Setdb1 did not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 ko resulted in ERV de-repression in both visceral and definitive endoderm cells, while H3K9me3 was unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 in ERV silencing in endoderm cells. Our findings suggest, that H3K9me3 is not sufficient for ERV silencing, but rather critical for maintaining high DNA methylation.
2022-08-01 | GSE169464 | GEO
Project description:During mammalian development DNA methylation patterns need to be reset in primordial germ cells (PGC) and preimplantation embryos. However, many retro-transposons and imprinted genes are resistant to such global epigenetic reprogramming via hitherto undefined mechanisms. Here, we report that some of these sequences are immune to widespread erasure of DNA methylation in the mouse embryonic stem cells (mESCs) lacking de novo DNA methyltransferases. Persistence of DNA methylation at these loci in mESCs depends on the histone H3K9 methyltransferase Setdb1, as deletion of Setdb1 results in reduction of H3K9me3 and DNA methylation levels concomitant with an increase in 5-hydroxymethylation (5hmC). In addition, depletion of H3K9 methyltransferase G9a leads to genome-wide reduction of DNA methylation but to a lesser extent at the above sequences. Taken together, these data reveal that Setdb1 ensures the fidelity of DNA methylation at specific loci in mESCs, which may reflect mechanisms functioning in vivo during key developmental stages. Examination of gene expression in 2 cell types by RNA-seq.
2014-06-03 | E-GEOD-47883 | biostudies-arrayexpress
Project description:During mammalian development DNA methylation patterns need to be reset in primordial germ cells (PGC) and preimplantation embryos. However, many retro-transposons and imprinted genes are resistant to such global epigenetic reprogramming via hitherto undefined mechanisms. Here, we report that some of these sequences are immune to widespread erasure of DNA methylation in the mouse embryonic stem cells (mESCs) lacking de novo DNA methyltransferases. Persistence of DNA methylation at these loci in mESCs depends on the histone H3K9 methyltransferase Setdb1, as deletion of Setdb1 results in reduction of H3K9me3 and DNA methylation levels concomitant with an increase in 5-hydroxymethylation (5hmC). In addition, depletion of H3K9 methyltransferase G9a leads to genome-wide reduction of DNA methylation but to a lesser extent at the above sequences. Taken together, these data reveal that Setdb1 ensures the fidelity of DNA methylation at specific loci in mESCs, which may reflect mechanisms functioning in vivo during key developmental stages. Examination of genome-wide DNA methylation status in 3 cell types.
2014-06-03 | E-GEOD-47890 | biostudies-arrayexpress