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Repression of endogenous retroviruses is required for mammary gland development and homeostasis [microarray]

ABSTRACT: Repression of endogenous retroviruses is required for mammary gland development and homeostasis [microarray]

PROVIDER: PRJNA713294 | ENA |

REPOSITORIES: ENA

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Repression of endogenous retroviruses is required for mammary gland development and homeostasis [microarray]

Project description:We demonstrate that loss of the histone H3K9 methyltransferase G9a in the developing mammary epithelium results in de novo chromatin opening which leads to severely impaired development of the mammary ductal tree, concomitant with impaired stem cell potential and disrupted intraductal polarity. Intriguingly, these phenotypes are not attributed to alterations in lineage specification and fidelity of the basal and luminal cell fates. Instead, increased chromatin opening in G9a-ablated mammary epithelium results in derepression of Long Terminal Repeat (LTR) sequences, most prominently of the ERVK family. When reverse-transcribed, these endogenous retroviruses generate double-stranded DNA (dsDNA) that accumulates in the cytosol of G9acKO mammary epithelial cells and trigger a pyroptotic antiviral innate immune response within mammary fat pads. Importantly, this altered G9acKO mammary milieu precludes functional outgrowth of even wild-type mammary stem cells upon transplantation. Our results show that tight repression of endogenous retroviruses is required for proper mammary gland development and maintenance. We demonstrate that altering chromatin accessibility of retroviral elements, as occurs during aging and cancer, severely disrupts functional mammary gland development and mammary stem cell activity through both cell autonomous and cell non-autonomous mechanisms.

2021-05-18 | GSE168624 | GEO

Repression of endogenous retroviruses is required for mammary gland development and homeostasis [ATAC-Seq]

2021-05-18 | GSE149977 | GEO

Repression of endogenous retroviruses is required for mammary gland development and homeostasis [RNA-Seq]

2021-05-18 | GSE149976 | GEO

Repression of endogenous retroviruses is required for mammary gland development and homeostasis [scRNA-Seq]

2021-05-18 | GSE149953 | GEO

Repression of endogenous retroviruses is required for mammary gland development and homeostasis

Project description:Repression of endogenous retroviruses is required for mammary gland development and homeostasis

| PRJNA630715 | ENA

Repression of endogenous retroviruses is required for mammary gland development and homeostasis [ATAC-Seq]

Project description:Repression of endogenous retroviruses is required for mammary gland development and homeostasis [ATAC-Seq]

| PRJNA630717 | ENA

Repression of endogenous retroviruses is required for mammary gland development and homeostasis [RNA-Seq]

Project description:Repression of endogenous retroviruses is required for mammary gland development and homeostasis [RNA-Seq]

| PRJNA630719 | ENA

Repression of endogenous retroviruses is required for mammary gland development and homeostasis [scRNA-Seq]

Project description:Repression of endogenous retroviruses is required for mammary gland development and homeostasis [scRNA-Seq]

| PRJNA630720 | ENA

Repression of endogenous retroviruses is required for mammary gland development and homeostasis

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-18 | GSE149978 | GEO

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

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