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Control of meiotic recombination by cell cycle kinases

AutorBustamante-Jaramillo, Luisa; Martín-Castellanos, Cristina
Fecha de publicación2014
EditorFundación Ramón Areces
CitaciónRamón Areces Foundation International Symposium (2014)
ResumenMeiosis is a type of cellular division in which a single round of DNA replication is followed by two nuclear divisions, originating four haploid cells from a diploid parental one, and therefore reducing the chromosomal number to half. Homologous recombination is a hallmark of meiosis that is essential for the correct chromosome segregation and the generation of genetic variability. It is initiated by the formation of double-strand breaks (DSBs) in the DNA, carried out by a conserved topoisomeraselike protein Spo11 (Rec12 in fission yeast). Rec12 (Spo11) needs the collaboration of accessory proteins, among them the ones forming the pre-recombination SFT complex (Rec7, Rec24, and Rec15). Recombination occurs in the context of the synaptonemal complex (Linear Elements in fission yeast) formed by Rec10, Rec25, Rec27 and Mug20. LinEs determine where DSBs occur and serve as platform where Rec12-accessory proteins are loaded. To understand how DSB formation is controlled is crucial to know how genome integrity is maintained during meiosis. In particular, we are interested in how meiotic progression is coordinated with recombination, and how DSB formation is prevented until cells have completed DNA replication. This aspect of meiosis is largely unknown and few data have been only reported in budding yeast, where Mer2 (Rec15 in fission yeast) is regulated by CDK and DDK (conserved kinase involved in cell cycle progression) to activate DSB formation. Currently, we are studying how LinE-components and Rec12-accessory proteins are regulated by CDK and DDK activity, and also by Rad3 (DNA-damage checkpoint kinase). We are taking different approaches. We are studying the influence of these kinases activities in LinE organization and foci formation of Rec12-accessory proteins by cytology. In addition, we are generating mutants in consensus phosphorylation sites in Rec7 by these kinases to explore possible effects on the localization of protein as well as in recombination. Finally, we are studying the impact of different cyclin deletion mutants (regulatory subunits of the CDK activity) in recombination and DSB formation.
DescripciónResumen del póster presentado al Ramón Areces Foundation International Symposium: Cell Proliferation and Genome Integrity, celebrado en Santander (España) del 3 al 4 de abril de 2014.
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