DAZL targets during male meiotic prophase I
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ABSTRACT:
PROVIDER: PRJNA578054 | ENA |
REPOSITORIES: ENA
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Project description:ZFP541 ChIP-seq targets during male meiotic prophase
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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:DAZL's targets were identified via iCLIP in leptotene-synchronized postnatal testes.
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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.
2021-04-15 | GSE169575 | GEO
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.
2021-03-24 | GSE169482 | GEO
Project description:The meiosis-specific chromosomal events of homolog pairing, synapsis, and recombination occur over an extended meiotic prophase I. In this study, we show that, in mice, maintenance of an extended meiotic prophase I requires the gene Meioc, a germ-cell specific factor conserved in most metazoans. Using immunoprecipitation and quantitative mass spectrometry, we identify proteins that interact with MEIOC in the mouse germ line.
2017-03-27 | PXD005473 | Pride
Project description:During meiosis, germ cell and stage-specific components impose additional layers of regulation on the core cell cycle machinery to set up an extended G2 period termed meiotic prophase. In Drosophila males, meiotic prophase lasts 3.5 days, during which spermatocytes upregulate over 1800 genes and grow 25-fold. Previous work has shown that the cell cycle regulator Cyclin B (CycB) is subject to translational repression in immature spermatocytes, mediated by the RNA-binding protein Rbp4 and its partner Fest. Here, we show that the spermatocyte-specific protein Lut is required for translational repression of cycB in an 8-h window just before spermatocytes are fully mature. In males mutant for rbp4 or lut, spermatocytes enter and exit meiotic division 6-8 h earlier than in wild type. In addition, spermatocyte-specific isoforms of Syncrip (Syp) are required for expression of CycB protein in mature spermatocytes and normal entry into the meiotic divisions. Lut and Syp interact with Fest independent of RNA. Thus a set of spermatocyte-specific regulators choreograph the timing of expression of CycB protein during male meiotic prophase.
2023-11-12 | GSE247385 | GEO
Project description:During meiosis, germ cell and stage-specific components impose additional layers of regulation on the core cell cycle machinery to set up an extended G2 period termed meiotic prophase. In Drosophila males, meiotic prophase lasts 3.5 days, during which spermatocytes upregulate over 1800 genes and grow 25-fold. Previous work has shown that the cell cycle regulator Cyclin B (CycB) is subject to translational repression in immature spermatocytes, mediated by the RNA-binding protein Rbp4 and its partner Fest. Here, we show that the spermatocyte-specific protein Lut is required for translational repression of cycB in an 8-h window just before spermatocytes are fully mature. In males mutant for rbp4 or lut, spermatocytes enter and exit meiotic division 6-8 h earlier than in wild type. In addition, spermatocyte-specific isoforms of Syncrip (Syp) are required for expression of CycB protein in mature spermatocytes and normal entry into the meiotic divisions. Lut and Syp interact with Fest independent of RNA. Thus a set of spermatocyte-specific regulators choreograph the timing of expression of CycB protein during male meiotic prophase.
2023-11-12 | GSE247386 | GEO
Project description:In meiotic prophase, chromosomes are organized into compacted loop arrays to promote homolog pairing and recombination. Here, we probe the architecture of the mouse spermatocyte genome in early and late meiotic prophase using Hi-C. We show that early-prophase chromosomes are arranged as linear arrays of 0.8-1 Mb loops, which extend to 1.5-2 Mb in late prophase as chromosomes compact and homologs undergo synapsis. Topologically associating domains (TADs) are lost in meiotic prophase, suggesting that assembly of the meiotic chromosome axis dramatically reduces the dynamics of chromosome-associated cohesin complexes. While TADs are lost, physically-separated A and B compartments are maintained in meiotic prophase. Moreover, meiotic DNA breaks and inter-homolog crossovers preferentially form in the gene-dense A compartment, revealing a role for chromatin organization in meiotic recombination. Finally, direct detection of inter-homolog contacts genome-wide reveals the structural basis for homolog alignment and juxtaposition by the synaptonemal complex.
2018-11-17 | GSE122622 | GEO
Project description:The meiotic cohesin Rec8 is required for the stepwise segregation of chromosomes during the two rounds of meiotic division. By directly measuring chromosome compaction in living cells of the fission yeast Schizosaccharomyces pombe, we found an additional role for the meiotic cohesin in the compaction of chromosomes during meiotic prophase. In the absence of Rec8, chromosomes were decompacted relative to those of wild-type cells. Conversely, loss of the cohesin-associated protein Pds5 resulted in hyper-compaction. While this hyper-compaction requires Rec8, binding of Rec8 to chromatin was reduced in the absence of Pds5, indicating that Pds5 promotes chromosome association of Rec8. To explain these observations, we propose that meiotic prophase chromosomes are organized as chromatin loops emanating from a Rec8-containing axis; the absence of Rec8 disrupts the axis, resulting in disorganized chromosomes, whereas reduced Rec8 loading results in a longitudinally compacted axis with fewer attachment points and longer chromatin loops. Keywords: ChIP-chip analysis ChIP analysis of Rec8: In all cases, hybridization data for ChIP fraction was compared with that of SUP (supernatant) fraction. Pombe chromosome II, III array was used.
2010-07-01 | E-GEOD-5284 | biostudies-arrayexpress