Maintenance DNA methylation in pre-meiotic germ cells regulates meiotic prophase by facilitating homologous chromosome pairing
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ABSTRACT:
PROVIDER: PRJNA717032 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14063562_1.fastq.gz | Fastqsanger.gz | |||
| SRR14063562_2.fastq.gz | Fastqsanger.gz | |||
| SRR14063563_1.fastq.gz | Fastqsanger.gz | |||
| SRR14063563_2.fastq.gz | Fastqsanger.gz | |||
| SRR14063564_1.fastq.gz | Fastqsanger.gz |
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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:Maintenance DNA methylation in pre-meiotic germ cells regulates meiotic prophase by facilitating homologous chromosome pairing
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Project description:We comprehensively compared the chromatin structures and transcriptomes in successive substages of female and male mouse meiotic prophase by using sisHi-C and RNA-Seq methods. Interestingly, the transcriptional change happened earlier than chromatin structures reprograming that chromatin structures largely maintained the pre-meiotic condition in leptotene. Also, compartments and TADs gradually disappeared and then slowly recovered in both oocytes and spermatocytes. We characterized the events of homologous chromosomes pairing and found homologues adopted two sex-conserved pairing strategies prior to and after leptotene-to-zygotene transition, which firstly contacted more frequently in LINE enriched compartment B and then switched to SINE enriched compartment A. The sexual difference of transcriptome was most obvious in late meiotic prophase, which reflected in gamete morphology and function differences. We also complemented marker genes for each substage of oocytes and spermatocytes meiotic prophase, and predicted the sex-specific meiotic functional genes, whose mutation or deletion may cause sex different effects on fertility. In summary, this study revealed the sexual similarities and dimorphic of higher-order chromatin architecture, homologous pairing and transcriptome during meiotic prophase of both oogenesis and spermatogenesis.
2023-09-23 | GSE220303 | GEO
Project description:3D genome remodeling and homologous pairing during meiotic prophase of mouse oogenesis and spermatogenesis
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Project description:Homologous pairing and synapsis are essential in meiotic prophase I during spermatogenesis. However, the underlying mechanisms of how alternative splicing (AS) functions in homologous pairing and synapsis remain largely unclear. We reveal that SRSF1 is essential for gene expression and AS in homologous pairing and synapsis. Conditional knockout (cKO) of Srsf1 in mouse germ cells impaired homologous pairing and synapsis, leading to non-obstructive azoospermia (NOA). SRSF1 was required for initial homology recognition, telomere-led chromosome movement, and synaptonemal complex (SC) assembly. Moreover, SRSF1 interacted with TRA2B and U2AF2, directly binding and regulating the expression of Dmc1, Sycp1, Sun1, and Majin via AS to implement homologous pairing and synapsis during the meiotic prophase I program. Altogether, our data reveal the critical role of an SRSF1-mediated post-transcriptional regulatory mechanism in homologous pairing and synapsis during meiotic prophase I, providing a framework for elucidating the molecular mechanisms underlying the post-transcriptional network of male meiosis.
2024-01-09 | GSE227403 | GEO
Project description:Homologous pairing and synapsis are essential in meiotic prophase I during spermatogenesis. However, the underlying mechanisms of how alternative splicing (AS) functions in homologous pairing and synapsis remain largely unclear. We reveal that SRSF1 is essential for gene expression and AS in homologous pairing and synapsis. Conditional knockout (cKO) of Srsf1 in mouse germ cells impaired homologous pairing and synapsis, leading to non-obstructive azoospermia (NOA). SRSF1 was required for initial homology recognition, telomere-led chromosome movement, and synaptonemal complex (SC) assembly. Moreover, SRSF1 interacted with TRA2B and U2AF2, directly binding and regulating the expression of Dmc1, Sycp1, Sun1, and Majin via AS to implement homologous pairing and synapsis during the meiotic prophase I program. Altogether, our data reveal the critical role of an SRSF1-mediated post-transcriptional regulatory mechanism in homologous pairing and synapsis during meiotic prophase I, providing a framework for elucidating the molecular mechanisms underlying the post-transcriptional network of male meiosis.
2024-01-08 | GSE227303 | 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: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:Chromosomes pair and synapse with their homologous partners to segregate correctly at meiosis I. Association of telomeres with the LINC (Linker of Nucleoskeleton and Cytoskeleton) complex enables telomere-led chromosome movements and telomere bouquet formation, facilitating precise pairwise alignment of homologs. Here, we identify a direct interaction between SUN1 and Speedy A (SPDYA) and determine the crystal structure of human SUN1-SPDYA-CDK2 ternary complex. Analysis of meiosis prophase I process in SPDYA-binding-deficient SUN1 mutant mice reveals that the SUN1-SPDYA interaction is required for the telomere-LINC complex connection and the assembly of a ring-shaped telomere supramolecular architecture at the nuclear envelope, which is critical for efficient homologous pairing and synapsis. Overall, our results provide structural insights into meiotic telomere structure that is essential for meiotic prophase progression.
2021-04-08 | GSE155142 | GEO