About the Project
Significantly, works from the Esashi group revealed that one of essential DNA repair proteins, the RAD51 recombinase, prevents centromere fragility, in a manner dependent on its phosphorylation by polo-like kinase 1, a central mitotic kinase which is enriched at centromeres (1, 2, 3). In line with this finding, emerging evidence indicates the enrichment of several repair proteins at centromeres (4). However, the full picture of the mechanism maintaining centromere integrity remains a major question in the field.
This project tackles this fundamental question by exploiting a newly developed system that enables the identification of factors that accumulate at centromeres upon the induction of local damage. The study will be followed by the characterisation of identified factors using multidisciplinary approaches, such as biochemistry, genetics and microscopic analysis. The project offers a unique training opportunity for student to interact with a powerful team of experts in the fields of DNA repair, recombination and replication (Esashi) and centromere and kinetochore biology (Gruneberg).
2. Yata et al., (2014) BRCA2 coordinates the activities of cell-cycle kinases to promote genome stability Cell Reports 7,1547-1559
3. Wassing I.E. et al. (2020) The RAD51 recombinase protects mitotic chromatin in human cells BioRxiv (https://doi.org/10.1101/2020.08.11.246231)
4. Gao et al., (2018) C-BERST: defining subnuclear proteomic landscapes at genomic elements with dCas9–APEX2. Nature Methods 15, 433–436
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