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The variation of bivalent histone modifications were tested during germline stem cell differentiation [ChIP-seq]

ABSTRACT: The variation of bivalent histone modifications were tested during germline stem cell differentiation [ChIP-seq]

PROVIDER: PRJNA688247 | ENA |

REPOSITORIES: ENA

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The variation of bivalent histone modifications were tested during germline stem cell differentiation [ChIP-seq]

Project description:during in vitro spermatogenesis and transdifferentiation of female germline stem cells into haploid spermatid-like cells , the variation of bivalent histone modifications were tested

2022-01-12 | GSE163928 | GEO

The variation of bivalent histone modifications and 3D chromosome structure during germline stem cell differentiation

Project description:The variation of bivalent histone modifications and 3D chromosome structure during germline stem cell differentiation

| PRJNA688244 | ENA

SCML2 establishes germline-specific bivalent domains.

Project description:Bivalent domains marked with repressive H3K27me3 and activating H3K4me2/3 are a molecular signature of totipotency in stem cells and development. While bivalent domains are retained throughout the germline to recover totipotency in the next generation, the mechanisms establishing bivalent domains remains unknown. Here we demonstrate that a germline-specific Polycomb protein, SCML2, binds to chromatin containing hypomethylated DNA to induce H3K27me3, thereby initiating the establishment of germline-specific bivalent domains in mice. SCML2 regulates two distinct classes of autosomal bivalent domains, the first are maintained constitutively through spermatogenesis (Class I), and the second are specifically established during meiosis (Class II). In postmeiotic spermatids, the loss of H3K27me3 leads to an increase of H3K4me2/3 on bivalent domains and disorganization of pericentromic heterochromatin. We propose that SCML2 regulates dynamic bivalent domains in the germline as a molecular imprint to recover totipotency after fertilization.

2018-04-12 | GSE89502 | GEO

The variation of 3D Chromosome Structure were tested during germline stem cell differentiation [HiC]

Project description:During in vitro spermatogenesis and transdifferentiation of female germline stem cells into haploid spermatid-like cells , the variation of chromatin organization by using in situ Hi-C were tested

2022-01-12 | GSE163929 | GEO

Temporally-coordinated bivalent histone modifications of BCG1 enable fungal invasion and immune evasion

Project description:Bivalent histone modifications, including functionally opposite H3K4me3 and H3K27me3 marks simultaneously on the same nucleosome, control various cellular processes by fine-tuning the gene expression in eukaryotes. However, the role of bivalent histone modifications in fungal virulence remains elusive. Here, we report that bivalent chromatin modification of BCG1 (bivalent chromatin-marked gene1) is critical for Fusarium graminearum (Fg) successfully invading the host plant. By mapping the genome-wide landscape of H3K4me3 and H3K27me3 dynamic modifications in Fg during invasion, we identified the infection-related bivalent chromatin-marked genes (BCGs). BCG1, which encodes a xylanase containing a novel G/Q-rich motif, possessed the highest bivalent modification. We showed that the G/Q-rich motif of BCG1 is required for its xylanase activity and is essential for the full virulence of Fg. Intriguingly, this G/Q-rich motif can be recognized by pattern-recognition receptors (PRRs) to trigger plant immunity. Therefore, Fg tightly regulates BCG1 expression during different infection stages. During initial infection stages, Fg employs H3K4me3 modification to induce BCG1 expression required for host cell wall degradation. Upon breaching the cell wall barrier, this active chromatin state was reset to bivalency by co-modifying with H3K27me3, which enables epigenetic silencing of BCG1 to escape from host immune surveillance. Collectively, our study highlights how fungal pathogens deploy bivalent epigenetic modification to achieve temporally-coordinated activation and suppression of a critical fungal gene, thereby facilitating successful infection and host immunity evasion. This SuperSeries is composed of the SubSeries listed below.

2023-12-04 | GSE213962 | GEO

The variation of 3D Chromosome Structure were tested during germline stem cell differentiation [HiC]

Project description:The variation of 3D Chromosome Structure were tested during germline stem cell differentiation [HiC]

| PRJNA688248 | ENA

Poised chromatin and bivalent domains facilitate the mitosis-to-meiosis transition in the male germline

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

2015-06-18 | E-GEOD-69946 | biostudies-arrayexpress

Kmt2b conveys monovalent and bivalent H3K4me3 in spermatogonial stem cells at germline and embryonic promoters

Project description:The mammalian male germline is sustained by a pool of spermatogonial stem cells (SSCs) that can transmit both genetic and epigenetic information to offspring. However, the mechanisms underlying epigenetic transmission remain unclear. The histone methyltransferase Kmt2b is highly expressed in SSCs and required for the SSC-to-progenitor transition. At the stem cell stage, Kmt2b catalyzes H3K4me3 at bivalent H3K27me3-marked promoters as well as at promoters of a new class of genes lacking H3K27me3, which we call monovalent. Monovalent genes are mainly activated in late spermatogenesis while the bivalent genes are mainly not expressed until embryonic development. These data suggest that SSCs are epigenetically primed by Kmt2b in two distinguishable ways for the upregulation of gene expression during the spermatogenic program and through the male germline into the embryo. Because Kmt2b is also the major H3K4 methyltransferase for bivalent promoters in embryonic stem cells, we also propose that Kmt2b has the capacity to epigenetically prime stem cells.

2018-11-18 | GSE92677 | GEO