Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA171334 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR527214.fastq.gz | Fastqsanger.gz | |||
| SRR527215.fastq.gz | Fastqsanger.gz | |||
| SRR527216.fastq.gz | Fastqsanger.gz | |||
| SRR527217.fastq.gz | Fastqsanger.gz | |||
| SRR527218.fastq.gz | Fastqsanger.gz |
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Project description:The four mammalian Argonaute family members are thought to share redundant functions in the microRNA pathway, yet only AGO2 possesses the catalytic "slicer" function required for RNA interference. Whether AGO1, AGO3, or AGO4 possess specialized functions remains unclear. Here, we Series_summary = show that AGO4 localizes to spermatocyte nuclei during meiotic prophase I, specifically at sites of asynapsis and in the transcriptionally silenced XY sub-domain, the sex body. We generated Ago4 knockout mice and show that Ago4-/- spermatogonia initiate meiosis early, resulting from premature induction of retinoic acid-response genes. During prophase I, the sex body assembles incorrectly in Ago4-/- mice, leading to disrupted meiotic sex chromosome inactivation (MSCI). This is associated with a dramatic loss of microRNAs, >20% of which arise from the X chromosome. Loss of AGO4 results in increased AGO3 in spermatocytes, indicating some degree of redundancy. Thus, AGO4 regulates meiotic entry and MSCI in mammalian germ cells, implicating small RNA pathways in these processes.
2012-08-01 | GSE39652 | GEO
Project description:The four mammalian Argonaute family members are thought to share redundant functions in the microRNA pathway, yet only AGO2 possesses the catalytic "slicer" function required for RNA interference. Whether AGO1, AGO3, or AGO4 possess specialized functions remains unclear. Here, we Series_summary = show that AGO4 localizes to spermatocyte nuclei during meiotic prophase I, specifically at sites of asynapsis and in the transcriptionally silenced XY sub-domain, the sex body. We generated Ago4 knockout mice and show that Ago4-/- spermatogonia initiate meiosis early, resulting from premature induction of retinoic acid-response genes. During prophase I, the sex body assembles incorrectly in Ago4-/- mice, leading to disrupted meiotic sex chromosome inactivation (MSCI). This is associated with a dramatic loss of microRNAs, >20% of which arise from the X chromosome. Loss of AGO4 results in increased AGO3 in spermatocytes, indicating some degree of redundancy. Thus, AGO4 regulates meiotic entry and MSCI in mammalian germ cells, implicating small RNA pathways in these processes. mRNA transcripts were isolated and prepared using pachytene spermatocytes, pre-meiotic testes and other tissues from Ago4+/+ and Ago4-/- littermates and sequenced using Illumina HiSeq2000. small RNA transcripts were isolated and prepared using pachytene spermatocytes from adult Ago4+/+ and Ago4-/- littermates and sequenced using Illumina GAII.
2012-08-01 | E-GEOD-39652 | biostudies-arrayexpress
Project description:we identify Scml2, a subunit of a germ cell-specific polycomb repressive complex 1 (PRC1), as a critical epigenetic modifier that establishes the germline-specific epigenome through two distinct functions. One of these functions is in the stem cell phase of spermatogonia and the other is on meiotic sex chromosomes. During the stem cell phase of spermatogonia, Scml2 establishes Rnf2- dependent ubiquitination of H2A (Rnf2-ubH2A) as an epigenetic memory that subsequently ensures programmed repression of somatic genes during the late stages of spermatogenesis. Additionally, during meiosis, Scml2 interacts with M-NM-3H2AX and works downstream of the DNA damage response factor Mdc1 on the sex chromosomes and, contrary to autosomes, suppresses Rnf2-ubH2A for proper epigenetic programming of the sex chromosomes. Taken together, Scml2 positively regulates Rnf2-ubH2A on autosomes and negatively regulates Rnf2-ubH2A on the sex chromosomes to establish the germline-specific epigenome in spermatogenesis. Our study reveals a novel layer of epigenetic regulation in the male germline and adds further insight into the functionality of the polycomb proteins. RNA-seq and ChIP-seq analyses using wild-type and Scml2 KO spermatogenic cells
2015-02-19 | E-GEOD-55060 | biostudies-arrayexpress
Project description:Gametogenesis is dependent on the expression of germline-specific genes. However, it remains unknown how the germline epigenome is distinctly established from that of somatic lineages. Here we show that genes commonly expressed in somatic lineages and spermatogenesis-progenitor cells undergo repression in a genome-wide manner in late stages of the male germline and identify underlying mechanisms. SCML2, a germline-specific subunit of a Polycomb repressive complex 1 (PRC1), establishes the unique epigenome of the male germline through two distinct antithetical mechanisms. SCML2 works with PRC1 and promotes RNF2-dependent ubiquitination of H2A, thereby marking somatic/progenitor genes on autosomes for repression. Paradoxically, SCML2 also prevents RNF2-dependent ubiquitination of H2A on sex chromosomes during meiosis, thereby enabling unique epigenetic programming of sex chromosomes for male reproduction. Our results reveal divergent mechanisms involving a shared regulator by which the male germline epigenome is distinguished from that of the soma and progenitor cells.
2015-02-19 | GSE55060 | GEO
Project description:The male germline transcriptome changes dramatically during the mitosis-to-meiosis transition to activate late spermatogenesis genes and to transiently suppress genes commonly expressed in somatic lineages and spermatogenesis progenitor cells, termed somatic/progenitor genes. These changes reflect epigenetic regulation. Induction of late spermatogenesis genes during spermatogenesis is facilitated by poised chromatin established in the stem cell phases of spermatogonia, whereas silencing of somatic/progenitor genes during meiosis and postmeiosis is associated with formation of bivalent domains which also allows the recovery of the somatic/progenitor program after fertilization. Importantly, during spermatogenesis mechanisms of epigenetic regulation on sex chromosomes are different from autosomes: X-linked somatic/progenitor genes are suppressed by meiotic sex chromosome inactivation without deposition of H3K27me3. Our results suggest that bivalent H3K27me3 and H3K4me2/3 domains are not limited to developmental promoters (which maintain bivalent domains that are silent throughout the reproductive cycle), but also underlie reversible silencing of somatic/progenitor genes during the mitosis-to-meiosis transition in late spermatogenesis.
2015-06-18 | GSE69946 | GEO
Project description:The switch from mitosis to meiosis is a major transition that takes place during germ cell development. The precise sequence and the different gene expression programs activated during this process are only partly known. Here, we applied single-cell mRNA sequencing to interrogate the transcriptional changes that occur during the early steps of male germ cell differentiation. We isolated single cells from testes using a Dazl-GFP reporter mouse, which allowed us to focus on germ cells undergoing the mitotic to meiotic transition. We identified 4 distinct meiotic stages with unique transcriptome profiles and reconstructed the timeline of the meiotic entry in silico, from spermatogonia up to the pachytene stage, identifying transcriptional changes with an unprecedented resolution. This allowed us to characterize 3 major transitions in the meiotic prophase 1 of the male germline: meiotic entry, the meiotic sex chromosome inactivation (MSCI), and concomitant pachytene transcriptional activation. Meiotic entry is initiated following the downregulation of a tightly connected set of pluripotency factors and accompanied by a global transcriptional silencing. In contrast, during subsequent sex chromosome inactivation at the zygotene stage, gene silencing proceeds in a defined order, related to gene function.
2021-05-22 | GSE114788 | GEO
Project description:The male germline transcriptome changes dramatically during the mitosis-to-meiosis transition to activate late spermatogenesis genes and to transiently suppress genes commonly expressed in somatic lineages and spermatogenesis progenitor cells, termed somatic/progenitor genes. These changes reflect epigenetic regulation. Induction of late spermatogenesis genes during spermatogenesis is facilitated by poised chromatin established in the stem cell phases of spermatogonia, whereas silencing of somatic/progenitor genes during meiosis and postmeiosis is associated with formation of bivalent domains which also allows the recovery of the somatic/progenitor program after fertilization. Importantly, during spermatogenesis mechanisms of epigenetic regulation on sex chromosomes are different from autosomes: X-linked somatic/progenitor genes are suppressed by meiotic sex chromosome inactivation without deposition of H3K27me3. Our results suggest that bivalent H3K27me3 and H3K4me2/3 domains are not limited to developmental promoters (which maintain bivalent domains that are silent throughout the reproductive cycle), but also underlie reversible silencing of somatic/progenitor genes during the mitosis-to-meiosis transition in late spermatogenesis. 29 samples analyzed by ChIP-Seq
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Project description:The Multicopy Gene Sly Represses the Sex Chromosomes in the Male Mouse Germline after Meiosis
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Project description:H3K9 tri-methylation (H3K9me3) plays emerging roles in gene regulation, beyond its accumulation on pericentric constitutive heterochromatin. It remains a mystery why and how H3K9me3 undergoes dynamic regulation in male meiosis. Here, we identify a novel, critical regulator of H3K9 methylation and spermatogenic heterochromatin organization: the germline-specific protein ATF7IP2 (MCAF2). We show that, in male meiosis, ATF7IP2 amasses on autosomal and X pericentric heterochromatin, spreads through the entirety of the sex chromosomes, and accumulates on thousands of autosomal promoters and retrotransposon loci. On the sex chromosomes, which undergo meiotic sex chromosome inactivation (MSCI), the DNA damage response pathway recruits ATF7IP2 to X pericentric heterochromatin, where it facilitates the recruitment of SETDB1, a histone methyltransferase that catalyzes H3K9me3. In the absence of ATF7IP2, male germ cells are arrested in meiotic prophase. Analyses of ATF7IP2-deficient meiosis reveal the protein’s essential roles in the maintenance of MSCI, suppression of retrotransposons, and global activation of autosomal genes. We propose that ATF7IP2 is a downstream effector of the DDR pathway in meiosis that coordinates the organization of heterochromatin and gene regulation through the spatial regulation of SETDB1-mediated H3K9me3 deposition. We performed gene expression analysis using data obtained from RNA-seq of Atf7ip2+/+ and Atf7ip2-/- pachytene spermatocytes.
2024-02-14 | GSE244087 | GEO
Project description:H3K9 tri-methylation (H3K9me3) plays emerging roles in gene regulation, beyond its accumulation on pericentric constitutive heterochromatin. It remains a mystery why and how H3K9me3 undergoes dynamic regulation in male meiosis. Here, we identify a novel, critical regulator of H3K9 methylation and spermatogenic heterochromatin organization: the germline-specific protein ATF7IP2 (MCAF2). We show that, in male meiosis, ATF7IP2 amasses on autosomal and X pericentric heterochromatin, spreads through the entirety of the sex chromosomes, and accumulates on thousands of autosomal promoters and retrotransposon loci. On the sex chromosomes, which undergo meiotic sex chromosome inactivation (MSCI), the DNA damage response pathway recruits ATF7IP2 to X pericentric heterochromatin, where it facilitates the recruitment of SETDB1, a histone methyltransferase that catalyzes H3K9me3. In the absence of ATF7IP2, male germ cells are arrested in meiotic prophase. Analyses of ATF7IP2-deficient meiosis reveal the protein’s essential roles in the maintenance of MSCI, suppression of retrotransposons, and global activation of autosomal genes. We propose that ATF7IP2 is a downstream effector of the DDR pathway in meiosis that coordinates the organization of heterochromatin and gene regulation through the spatial regulation of SETDB1-mediated H3K9me3 deposition. CUT&RUN of H3K9me3 in Atf7ip2+/+ and Atf7ip2-/- pachytene spermatocytes and CUT&Tag of ATF7IP2 in C57/B6 WT pachytene spermatocytes.
2024-02-14 | GSE244083 | GEO