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SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice [RNA-seq]

ABSTRACT: SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice [RNA-seq]

PROVIDER: PRJNA944983 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23869511_1.fastq.gz	Fastqsanger.gz
	SRR23869511_2.fastq.gz	Fastqsanger.gz
	SRR23869512_1.fastq.gz	Fastqsanger.gz
	SRR23869512_2.fastq.gz	Fastqsanger.gz
	SRR23869513_1.fastq.gz	Fastqsanger.gz

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SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice [RNA-seq]

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

SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice [CLIP-seq]

2024-01-08 | GSE227303 | GEO

SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice

Project description:SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice

| PRJNA945019 | ENA

SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice [CLIP-seq]

Project description:SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice [CLIP-seq]

| PRJNA944606 | ENA

SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-09 | GSE227422 | GEO

The Essential Function of SETDB1 in Homologous Chromosome Pairing and Synapsis during Meiosis.

Project description:SETDB1 is a histone-lysine N-methyltransferase critical for germline development. However, its function in early meiotic prophase I remains unknown. Here, we report that Setdb1 null spermatocytes display aberrant centromere clustering during leptotene, bouquet formation during zygotene, and subsequent failure in pairing and synapsis of homologous chromosomes, as well as compromised meiotic silencing of unsynapsed chromatin, which leads to meiotic arrest before pachytene and apoptosis of spermatocytes. H3K9me3 is enriched in centromeric or pericentromeric regions and is present in many sites throughout the genome, with a subset changed in the Setdb1 mutant. These observations indicate that SETDB1-mediated H3K9me3 is essential for the bivalent formation in early meiosis. Transcriptome analysis reveals the function of SETDB1 in repressing transposons and transposon-proximal genes and in regulating meiotic and somatic lineage genes. These findings highlight a mechanism in which SETDB1-mediated H3K9me3 during early meiosis ensures the formation of homologous bivalents and survival of spermatocytes.

| S-EPMC8513770 | biostudies-literature

PAR-TERRA RNA directs homologous sex chromosome pairing

Project description:In mammals, homologous chromosomes rarely pair outside meiosis. One exception is the X chromosome, which transiently pairs during X-chromosome inactivation (XCI). How two chromosomes find each other in 3D space is not known. Here, we reveal a required interaction between the X-inactivation center (Xic) and the telomere in mouse embryonic stem (ES) cells. The subtelomeric, pseudoautosomal regions (PARs) of the two sex chromosomes (X and Y) also undergo pairing in both female and male cells. PARs transcribe a class of telomeric RNA, dubbed PAR-TERRA, which accounts for a vast majority of all TERRA transcripts. PAR-TERRA binds throughout the genome, including to the PAR and Xic. During X-chromosome pairing, PAR-TERRA anchors the Xic to the PAR, creating a ‘tetrad’ of pairwise homologous interactions (Xic–Xic, PAR–PAR, and Xic–PAR). Xic pairing occurs within the tetrad. Depleting PAR-TERRA abrogates pairing and blocks initiation of XCI, whereas autosomal PAR-TERRA induces ectopic pairing. We propose a ‘constrained diffusion model’ in which PAR-TERRA creates an interaction hub to guide Xic homology searching during XCI.

2017-07-10 | GSE69887 | GEO

SRSF1 regulates primordial follicle formation and number determination during meiotic prophase I

Project description:Serine/arginine-rich splicing factor 1 (SRSF1; previously SF2/ASF) is a pivotal posttranscriptional regulator of gene expression in various biological processes. However, the physiological roles and mechanism of SRSF1 in mouse early-stage oocytes remain elusive. Here we show that SRSF1 is essential for primordial follicle formation and number determination during meiotic prophase I. The conditional knockout of Srsf1 in mouse oocytes impairs primordial follicle formation and leads to primary ovarian insufficiency (POI). Oocyte-specific genes (e.g., LHX8, NOBOX, SOHLH1, SOHLH2, FIGLA, KIT, JAGGED1, and RAC1) that regulate primordial follicle formation are suppressed in newborn Stra8-GFPCre Srsf1Fl/Fl (cKO) mouse ovaries. However, meiotic defects are the leading cause of abnormal primordial follicle formation. In cKO mouse ovaries, immunofluorescence results suggest that the failure of synapsis and the inability to undergo recombination result in fewer homologous DNA crossovers (COs). Moreover, SRSF1 directly binds and regulates the expression of the POI-related genes Six6os1 and Msh5 via alternative splicing to implement the meiotic prophase I program. Altogether, our data reveal a critical role of the SRSF1-mediated posttranscriptional regulatory mechanism in the mouse oocyte meiotic prophase I program, which provides a framework to elucidate molecular mechanisms of the posttranscriptional network underlying primordial follicle formation.

2023-02-06 | GSE198205 | GEO

Maintenance DNA methylation in pre-meiotic germ cells regulates meiotic prophase by facilitating homologous chromosome pairing

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

Maintenance DNA methylation in pre-meiotic germ cells regulates meiotic prophase by facilitating homologous chromosome pairing

2021-04-15 | GSE169575 | GEO