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Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at meiotic promoters in mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE295991 | GEO | 2025/05/10

REPOSITORIES: GEO

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Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [CUT&RUN]

Project description:Meiotic prophase I characterized by homologous recombination and synapsis is an intricate step for spermatogenesis. This process entails extensive changes to chromatin and transcription. Recent studies have revealed that prior to prophase I, accessible chromatin bound by paused Pol II at meiotic gene promoters is essential for their timely activation during later stages of prophase I. However, the factor responsible for promoting accessible chromatin at meiotic gene promoters before entry into prophase I is unknown. Here, we discovered that NFYA expressed in pre-meiotic germ cells promotes accessible chromatin at meiotic gene promoters. Concordantly, conditional germline deletion of Nfya in male mice blocks meiotic entry. Functionally, our spatial and single-cell ATAC-seq data revealed that loss of NFYA in pre-meiotic cells disrupts accessible chromatin at meiotic gene promoters. Our study identifies a pioneer role for NFYA in facilitating permissive chromatin at meiotic gene promoters before meiosis, thereby controlling the timely activation of meiotic genetic program during later meiosis.

2025-05-10 | GSE295964 | GEO

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [ATAC-seq]

2025-05-10 | GSE295941 | GEO

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [scRNA-seq & scATAC-seq]

2025-05-10 | GSE296438 | GEO

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at meiotic promoters in mice

Project description:Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at meiotic promoters in mice

| PRJNA1257271 | ENA

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [CUT&RUN]

Project description:Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [CUT&RUN]

| PRJNA1256871 | ENA

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [ATAC-seq]

Project description:Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [ATAC-seq]

| PRJNA1256837 | ENA

Control of meiotic entry by dual inhibition of a key mitotic transcription factor.

Project description:The mitosis to meiosis transition requires dynamic changes in gene expression, but whether and how the mitotic transcriptional machinery is regulated during this transition is unknown. In budding yeast, SBF and MBF transcription factors initiate the mitotic gene expression program. Here, we report two mechanisms that work together to restrict SBF activity during meiotic entry: repression of the SBF-specific Swi4 subunit through LUTI-based regulation and inhibition of SBF by Whi5, a functional homolog of the Rb tumor suppressor. We find that untimely SBF activation causes downregulation of early meiotic genes and delays meiotic entry. These defects are largely driven by the SBF-target G1 cyclins, which block the interaction between the central meiotic regulator Ime1 and its cofactor Ume6. Our study provides insight into the role of SWI4LUTI in establishing the meiotic transcriptional program and demonstrates how the LUTI-based regulation is integrated into a larger regulatory network to ensure timely SBF activity.

| S-EPMC10939502 | biostudies-literature

ATF7IP2/MCAF2 directs H3K9 methylation and meiotic gene regulation in the male germline.

Project description:H3K9 trimethylation (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 I. Analyses of ATF7IP2-deficient meiosis reveal the protein's essential roles in the maintenance of MSCI, suppression of retrotransposons, and global up-regulation 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.

| S-EPMC10982687 | biostudies-literature

ATF7IP2/MCAF2 directs H3K9 methylation and meiotic gene regulation in the male germline.

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 I. Analyses of ATF7IP2-deficient meiosis reveal the protein's essential roles in the maintenance of MSCI, suppression of retrotransposons, and global upregulation 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.

| S-EPMC10592865 | biostudies-literature

Project description:Approximately 10% of genes in the human genome are distributed such that their transcription start sites are located less than 1 kb apart on opposite strands. These divergent gene pairs have a single intergenic segment of DNA, which in some cases appears to share regulatory elements, but it is unclear whether these regions represent functional bidirectional promoters or two overlapping promoters. A recent study showed that divergent promoters are enriched for consensus binding sequences of a small group of transcription factors, including the ubiquitous ets-family transcription factor GA-binding protein (GABP). Here we show that GABP binds to more than 80% of divergent promoters in at least one cell type. Furthermore, we demonstrate that GABP binding is correlated and associated with bidirectional transcriptional activity in a luciferase transfection assay. In addition, we find that the addition of a strict consensus GABP site into a set of promoters that normally function in only one direction significantly increases activity in the opposite direction in 67% of cases. Our findings demonstrate that GABP regulates the majority of divergent promoters and suggest that bidirectional transcriptional activity is mediated through GABP binding and transactivation at both divergent and nondivergent promoters.

| S-EPMC2077898 | biostudies-literature

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