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Proc Natl Acad Sci U S A ; 119(21): e2117865119, 2022 05 24.
Artículo en Inglés | MEDLINE | ID: mdl-35576467

RESUMEN

Crossover formation is essential for proper segregation of homologous chromosomes during meiosis. Here, we show that Caenorhabditis elegans cyclin-dependent kinase 2 (CDK-2) partners with cyclin-like protein COSA-1 to promote crossover formation by promoting conversion of meiotic double-strand breaks into crossover­specific recombination intermediates. Further, we identify MutSγ component MSH-5 as a CDK-2 phosphorylation target. MSH-5 has a disordered C-terminal tail that contains 13 potential CDK phosphosites and is required to concentrate crossover­promoting proteins at recombination sites. Phosphorylation of the MSH-5 tail appears dispensable in a wild-type background, but when MutSγ activity is partially compromised, crossover formation and retention of COSA-1 at recombination sites are exquisitely sensitive to phosphosite loss. Our data support a model in which robustness of crossover designation reflects a positive feedback mechanism involving CDK-2­mediated phosphorylation and scaffold-like properties of the MSH5 C-terminal tail, features that combine to promote full recruitment and activity of crossover­promoting complexes.


Asunto(s)
Proteínas de Caenorhabditis elegans , Quinasa 2 Dependiente de la Ciclina , Proteínas de Unión al ADN , Meiosis , Complejo Sinaptonémico , Animales , Caenorhabditis elegans/genética , Caenorhabditis elegans/metabolismo , Proteínas de Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/metabolismo , Segregación Cromosómica , Intercambio Genético , Quinasa 2 Dependiente de la Ciclina/genética , Quinasa 2 Dependiente de la Ciclina/metabolismo , Proteínas de Unión al ADN/metabolismo , Fosforilación , Complejo Sinaptonémico/genética , Complejo Sinaptonémico/metabolismo
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