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The Role of cohEsin dynamicS at sTAlled ReplicaTion forks
Cohesin, an evolutionary conserved ring-shaped protein complex that topologically entraps DNA, has crucial roles in many structural and functional aspects of chromosomes including sister chromatid cohesion, genome organization, ge...
Cohesin, an evolutionary conserved ring-shaped protein complex that topologically entraps DNA, has crucial roles in many structural and functional aspects of chromosomes including sister chromatid cohesion, genome organization, gene transcription and DNA repair. The importance of cohesin in the maintenance of genomic stability has been known for some time. Cohesin facilitates double strand breaks repair by homologous recombination and promotes the restart of stalled replication forks by template switching, an error-free DNA tolerance pathway. However, the precise role of cohesin in DNA damage and in the recovery after replication stress is still unknown. Whether cohesin acts exclusively providing close proximity of sister chromatids or its functions exceed simple embracing of DNA has yet to be discerned. Cohesin has been shown to be ubiquitylated upon replication fork arrest. This post-translational modification has been proposed to favour cohesin mobilization and subsequent association with nascent DNA behind the fork. However, the extent to what cohesin dynamics are important in the recovery after replication stress is still to be understood. By a range of multidisciplinary approaches, from biochemistry and enzymology, yeast genetics and molecular biology techniques to high throughput proteomics and bioinformatics analysis of mass spectrometry data, we will gain valuable insight about the interplay between sister chromatid cohesion and DNA damage tolerance and their contribution to successful replication. This basic knowledge about the mechanisms involved in DNA damage responses has demonstrated to be essential in the design of successful strategies against cancer. Remarkably, cohesin is one of the protein complexes most frequently mutated in cancer. This project aims to provide valuable insight about how cohesin mutations cause tumorigenesis.
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Duración del proyecto: 29 meses
Fecha Inicio: 2023-05-03
Fecha Fin: 2025-10-31
Fecha Fin: 2025-10-31
Línea de financiación: concedida
El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2023-05-03
Línea de financiación objetivo
El proyecto se financió a través de la siguiente ayuda:
HORIZON-MSCA-2022-PF-01-01:
MSCA Postdoctoral Fellowships 2022
Cerrada
hace 2 años
Presupuesto
El presupuesto total del proyecto asciende a
181K€
Líder del proyecto
UNIVERSIDAD DE SALAMANCA
No se ha especificado una descripción o un objeto social para esta compañía.
Total investigadores
1148
Total investigadores
1148