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Overlapping and separable activities of BRA-2 and HIM-17 promote occurrence and regulation of pairing and synapsis during Caenorhabditis elegans meiosis

ABSTRACT: Overlapping and separable activities of BRA-2 and HIM-17 promote occurrence and regulation of pairing and synapsis during Caenorhabditis elegans meiosis

PROVIDER: PRJNA1152551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30400044_1.fastq.gz	Fastqsanger.gz
	SRR30400044_2.fastq.gz	Fastqsanger.gz
	SRR30400045_1.fastq.gz	Fastqsanger.gz
	SRR30400045_2.fastq.gz	Fastqsanger.gz
	SRR30400046_1.fastq.gz	Fastqsanger.gz

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Overlapping and separable activities of BRA-2 and HIM-17 promote occurrence and regulation of pairing and synapsis during Caenorhabditis elegans meiosis

Project description:Faithful meiotic segregation requires pairwise alignment of the homologous chromosomes and their synaptonemal complex (SC) mediated stabilization. Here, we investigate on new factors that promote and coordinate these events during C. elegans meiosis. We identify BRA-2 (BMP Receptor Associated family member 2) as an interactor of HIM-17, previously shown to promote double-strand break formation. We found that loss of bra-2 impairs synapsis elongation without affecting homolog recognition, chromosome movement or SC maintenance. Epistasis analyses reveal previously unrecognized activities for HIM-17 in regulating homolog paring and SC assembly in a partially overlapping manner with BRA-2. We show that removing bra-2 or him-17 restores nuclear clustering, recruitment of PLK-2 at the nuclear periphery and abrogation of ectopic synapsis in htp-1 mutants, suggesting intact CHK-2-mediated signaling and presence of a barrier that prevents SC polymerization in absence of homology. Our findings shed new light on the regulatory mechanisms ensuring faithful pairing and synapsis.

2025-01-22 | GSE275668 | GEO

Distinct intersecting pathways link homolog pairing to initiation of meiotic chromosome synapsis

Project description:Faithful meiotic segregation requires pairwise alignment of the homologous chromosomes and Synaptonemal Complex assembly (SC) at their interface. Here, we investigate on new factors that promote and coordinate these events during C. elegans meiosis. We identify BRA-2 (BMP Receptor Associated family member 2) as an interactor of HIM-17, previously shown to promote double-strand break formation. We found that loss of bra-2 specifically impairs synapsis licensing without affecting homologs recognition, SC maintenance or chromosome movement. Double mutant analysis revealed a previously unrecognized role for HIM-17 in promoting homolog pairing under dysfunctional SC assembly, without perturbing nuclear envelope recruitment of factors required for chromosome movement. We provide evidence that bra-2 and him-17 act in distinct pathways, exerting partially redundant functions in SC licensing, as well as separable roles in regulating homologs pairing. Altogether, our findings unveil novel mechanisms that ensure stabilization of homologous chromosome interaction via SC licensing upon homology assessment.

2025-03-14 | PXD053401 | Pride

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

2024-01-08 | GSE227303 | GEO

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

2024-01-09 | GSE227403 | GEO

Overlapping and separable activities of BRA-2 and HIM-17 promote occurrence and regulation of pairing and synapsis during Caenorhabditis elegans meiosis.

Project description:Faithful meiotic segregation requires pairwise alignment of the homologous chromosomes and their synaptonemal complex (SC) mediated stabilization. Here, we investigate factors that promote and coordinate these events during C. elegans meiosis. We identify BRA-2 (BMP Receptor Associated family member 2) as an interactor of HIM-17, previously shown to promote double-strand break formation. We found that loss of bra-2 impairs synapsis elongation without affecting homolog recognition, chromosome movement or SC maintenance. Epistasis analyses reveal previously unrecognized activities for HIM-17 in regulating homolog pairing and SC assembly in a partially overlapping manner with BRA-2. We show that removing bra-2 or him-17 restores nuclear clustering, recruitment of PLK-2 at the nuclear periphery, and abrogation of ectopic synapsis in htp-1 mutants, suggesting intact CHK-2-mediated signaling and presence of a barrier that prevents SC polymerization in the absence of homology. Our findings shed light on the regulatory mechanisms ensuring faithful pairing and synapsis.

| S-EPMC11906835 | biostudies-literature

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

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

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

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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

Integrative Structural Model of DNA-PK Synapsis

Project description:In non-homologous end joining repair of DNA double strand breaks, DNA dependent protein kinase catalytic subunit (DNA-PKcs) and Ku70/80 binds the free DNA ends forming the holoenzyme DNA-PK. DNA-PK synapses across the break to tether the broken ends in the initial long range synaptic complex. We generated an integrative structural model of DNA-PK synapsis at a precision of 13.5Å with crosslinking mass spectrometry (XL-MS) restraints. While our hydrogen deuterium exchange (HX) analysis revealed an allosteric axis in DNA-PK connecting DNA binding (including the plug domain) to the kinase domain. Our model presents a symmetrical synapsis primarily through head to head interactions and protection of the DNA by previously uncharacterized a plug domain. The offset of the DNA in our model allows access to downstream processing enzymes, while the combination of DNA binding and kinase loading creates a tensed state that could have roles in the re-arrangement/dissociation of DNA-PKcs as the repair process progresses.

2021-01-20 | PXD017931 | Pride

BCAS2 and hnRNPH1 orchestrate alternative splicing for DNA double-strand break repair and synapsis in meiotic prophase I [RNAs-seq]

Project description:Understanding the intricacies of homologous recombination during meiosis is crucial for reproductive biology. However, the role of alternative splicing (AS) in DNA double-strand breaks (DSBs) repair and synapsis remains elusive. In this study, we investigated the impact of conditional knockout (cKO) of the splicing factor gene Bcas2 in mouse germ cells, revealing impaired DSBs repair and synapsis, resulting in non-obstructive azoospermia (NOA). Employing crosslinking immunoprecipitation and sequencing (CLIP-seq), we globally mapped BCAS2 binding sites in the testis, uncovering its predominant association with 5' splice sites (5'SS) of introns and a preference for GA-rich regions. Integrating CLIP-seq with RNA-seq, we identified BCAS2 as a key player in the AS of pre-mRNAs, including Spo11, Six6os1, Sycp1, Msh5, Cdk2, Sun2, Stag3, and Spdya, crucial for DSBs repair and synapsis. Notably, BCAS2 exhibited direct binding and regulatory influence on Trp53bp1 and Six6os1 through AS, unveiling novel insights into DSBs repair and synapsis during meiotic prophase I. Furthermore, the interaction between BCAS2, hnRNPH1, and SRSF3 was discovered to orchestrate Trp53bp1 expression via AS, underscoring its role in meiotic prophase I DSBs repair. In summary, our findings delineate the indispensable role of BCAS2-mediated post-transcriptional regulation in DSBs repair and synapsis during male meiosis. This study provides a comprehensive framework for unraveling the molecular mechanisms governing the post-transcriptional network in male meiosis, contributing to the broader understanding of reproductive biology.

2024-03-25 | GSE254463 | GEO

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