ZFP541 ChIP-seq targets during male meiotic prophase
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA688209 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13313083.fastq.gz | Fastqsanger.gz | |||
| SRR13313084.fastq.gz | Fastqsanger.gz | |||
| SRR13313085.fastq.gz | Fastqsanger.gz |
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Project description:ZFP541 is assumed to possess putative DNA-binding domains and associated with histone deacetylases, implying it plays a role in regulation of transcription via modulation of chromatin status. Therefore, we used ChIP-seq to search for targets of ZFP541 in meiotic prophase of mouse spermatocytes.
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Project description:ZFP541 is one of the candidates for a transcriptional regulator during mouse meiotic prophase. In order to address the role of ZFP541, transcriptomes of meiotic prophase-enriched population were compared between Zfp541 +/- and Zfp541 KO testes by RNA-seq. The meiotic prophase-enriched population was isolated from Zfp541 +/- and Zfp541 KO testes at postnatal day 18 (P18), on the Rec8-3FH-GFP KI background by fluorescent sorting of GFP positive cells.
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Project description:Due to the DNA binding affinity and interacting ability with HDACs, we wonder if ZFP541 can regulate gene expression during meiotic prophase.
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Project description:The DSB-machinery, which induces the programmed DNA double-strand breaks (DSBs) in leptotene and zygotene stages during meiosis, needs to be kept in silence after the initiation of pachytene stage to prevent the activation of DSB checkpoint that may lead to meiotic arrest or apoptosis of germ cells. However, the mechanisms underlying this repression remain largely unknown. Here, we report that ZFP541, a germ cell-specific zinc finger protein, is responsible for the suppression of DSBs formation at late pachytene. Lack of Zfp541 in mice leads to generation of DSBs in late pachytene spermatocytes by DSB formation related-proteins and causes male infertility due to meiotic failure. Plated-based scRNA-seq of Zfp541-/- spermatocytes revealed that ZFP541 negatively regulates many meiotic prophase genes, including genes for DSB formation and their upstream transcriptional regulators, in late pachytene spermatocytes. These results were confirmed by 10x single-cell RNA-seq data on spermatogenesis of Zfp541-/- testes, which suggested that Zfp541 is required for repressing the activation of pre-pachytene gene expression programs from early to late pachytene. ZFP541 ChIP-seq on pachytene and diplotene spermatocytes demonstrated that ZFP541 occupies the promoters of meiosis initiators (e.g., Meiosin and Rxra) and a subset of their downstream genes to repress their transcription, and thus prevent the reactivation of pre-pachytene gene expression programs in pachytene spermatocytes. Thus, our results not only revealed the role of ZFP541 in maintaining the repression of pre-pachytene transcriptional programs in pachytene spermatocytes but also provide new insight into the regulation of meiotic progression by timely turning off pre-pachytene genes.
2021-04-16 | GSE172160 | GEO
Project description:The DSB-machinery, which induces the programmed DNA double-strand breaks (DSBs) in leptotene and zygotene stages during meiosis, needs to be kept in silence after the initiation of pachytene stage to prevent the activation of DSB checkpoint that may lead to meiotic arrest or apoptosis of germ cells. However, the mechanisms underlying this repression remain largely unknown. Here, we report that ZFP541, a germ cell-specific zinc finger protein, is responsible for the suppression of DSBs formation at late pachytene. Lack of Zfp541 in mice leads to generation of DSBs in late pachytene spermatocytes by DSB formation related-proteins and causes male infertility due to meiotic failure. Plated-based scRNA-seq of Zfp541-/- spermatocytes revealed that ZFP541 negatively regulates many meiotic prophase genes, including genes for DSB formation and their upstream transcriptional regulators, in late pachytene spermatocytes. These results were confirmed by 10x single-cell RNA-seq data on spermatogenesis of Zfp541-/- testes, which suggested that Zfp541 is required for repressing the activation of pre-pachytene gene expression programs from early to late pachytene. ZFP541 ChIP-seq on pachytene and diplotene spermatocytes demonstrated that ZFP541 occupies the promoters of meiosis initiators (e.g., Meiosin and Rxra) and a subset of their downstream genes to repress their transcription, and thus prevent the reactivation of pre-pachytene gene expression programs in pachytene spermatocytes. Thus, our results not only revealed the role of ZFP541 in maintaining the repression of pre-pachytene transcriptional programs in pachytene spermatocytes but also provide new insight into the regulation of meiotic progression by timely turning off pre-pachytene genes.
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Project description:The DSB-machinery, which induces the programmed DNA double-strand breaks (DSBs) in leptotene and zygotene stages during meiosis, needs to be kept in silence after the initiation of pachytene stage to prevent the activation of DSB checkpoint that may lead to meiotic arrest or apoptosis of germ cells. However, the mechanisms underlying this repression remain largely unknown. Here, we report that ZFP541, a germ cell-specific zinc finger protein, is responsible for the suppression of DSBs formation at late pachytene. Lack of Zfp541 in mice leads to generation of DSBs in late pachytene spermatocytes by DSB formation related-proteins and causes male infertility due to meiotic failure. Plated-based scRNA-seq of Zfp541-/- spermatocytes revealed that ZFP541 negatively regulates many meiotic prophase genes, including genes for DSB formation and their upstream transcriptional regulators, in late pachytene spermatocytes. These results were confirmed by 10x single-cell RNA-seq data on spermatogenesis of Zfp541-/- testes, which suggested that Zfp541 is required for repressing the activation of pre-pachytene gene expression programs from early to late pachytene. ZFP541 ChIP-seq on pachytene and diplotene spermatocytes demonstrated that ZFP541 occupies the promoters of meiosis initiators (e.g., Meiosin and Rxra) and a subset of their downstream genes to repress their transcription, and thus prevent the reactivation of pre-pachytene gene expression programs in pachytene spermatocytes. Thus, our results not only revealed the role of ZFP541 in maintaining the repression of pre-pachytene transcriptional programs in pachytene spermatocytes but also provide new insight into the regulation of meiotic progression by timely turning off pre-pachytene genes.
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Project description:During spermatogenesis, mammalian spermatogonia undergo mitotic division, to maintain stem cell pool via self-renewal and generate differentiating progenitor cells for entry into meiotic prophase. During the perinatal stage, de novo DNA methylation occurring in pro-spermatogonia plays a key role to complete meiotic prophase and initiate meiotic division. In contrast, the role of the maintenance DNA methylation pathway for regulation of meiotic prophase, or meiotic division, in the adult is not well understood. Here, by using conditional mutants for Np95 (nuclear protein 95 kDa, also known as Uhrf1) or Dnmt1 [DNA (cytosine-5)-methyltransferase 1], two proteins that are essential for maintenance DNA methylation, we reveal that both NP95 and DNMT1 are co-expressed in spermatogonia and that these factors are necessary for meiosis in male germ cells. We found that Np95- or Dnmt1-deficient spermatocytes exhibited spermatogenic defects involving synaptic failure during meiotic prophase. In addition, assembly of pericentric heterochromatin clusters in early meiotic prophase, a phenomenon that is required for subsequent pairing of homologous chromosomes, is disrupted in Np95-deficient as well as Dnmt1-deficient spermatocytes. Based on these observations, we propose that DNA methylation established in pre-meiotic spermatogonia regulates synapsis of homologous chromosomes, and in turn quality control of male germ cells. Maintenance DNA methylation, therefore, plays a role to ensure faithful transmission of both genetic and epigenetic information to offspring.
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Project description:During spermatogenesis, mammalian spermatogonia undergo mitotic division, to maintain stem cell pool via self-renewal and generate differentiating progenitor cells for entry into meiotic prophase. During the perinatal stage, de novo DNA methylation occurring in pro-spermatogonia plays a key role to complete meiotic prophase and initiate meiotic division. In contrast, the role of the maintenance DNA methylation pathway for regulation of meiotic prophase, or meiotic division, in the adult is not well understood. Here, by using conditional mutants for Np95 (nuclear protein 95 kDa, also known as Uhrf1) or Dnmt1 [DNA (cytosine-5)-methyltransferase 1], two proteins that are essential for maintenance DNA methylation, we reveal that both NP95 and DNMT1 are co-expressed in spermatogonia and that these factors are necessary for meiosis in male germ cells. We found that Np95- or Dnmt1-deficient spermatocytes exhibited spermatogenic defects involving synaptic failure during meiotic prophase. In addition, assembly of pericentric heterochromatin clusters in early meiotic prophase, a phenomenon that is required for subsequent pairing of homologous chromosomes, is disrupted in Np95-deficient as well as Dnmt1-deficient spermatocytes. Based on these observations, we propose that DNA methylation established in pre-meiotic spermatogonia regulates synapsis of homologous chromosomes, and in turn quality control of male germ cells. Maintenance DNA methylation, therefore, plays a role to ensure faithful transmission of both genetic and epigenetic information to offspring.
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