Overlapping and separable activities of BRA-2 and HIM-17 promote occurrence and regulation of pairing and synapsis during Caenorhabditis elegans meiosis
Jazyk angličtina Země Anglie, Velká Británie Médium electronic
Typ dokumentu časopisecké články
Grantová podpora
GA23-04918S
Grantová Agentura České Republiky (Grant Agency of the Czech Republic)
PubMed
40082424
PubMed Central
PMC11906835
DOI
10.1038/s41467-025-57862-y
PII: 10.1038/s41467-025-57862-y
Knihovny.cz E-zdroje
- MeSH
- Caenorhabditis elegans * genetika metabolismus cytologie MeSH
- meióza * genetika fyziologie MeSH
- mutace MeSH
- párování chromozomů * genetika MeSH
- proteiny buněčného cyklu * metabolismus genetika MeSH
- proteiny Caenorhabditis elegans * metabolismus genetika MeSH
- synaptonemální komplex metabolismus genetika MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- Htp-1 protein, C elegans MeSH Prohlížeč
- proteiny buněčného cyklu * MeSH
- proteiny Caenorhabditis elegans * MeSH
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.
Department of Biology Faculty of Medicine Masaryk University Brno Czech Republic
Department of Biology Faculty of Science McGill University Montreal QC Canada
Department of Biology University of Iowa Iowa City IA USA
Department of Biomedical Informatics University of Pittsburgh School of Medicine Pittsburgh PA USA
Magee Womens Research Institute Pittsburgh PA USA
Max Perutz Labs Vienna Biocenter Campus Vienna Biocenter Vienna Austria
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