Supervisore: Prof. Brancolini

Investigation of epigenetic mechanisms that supervise HR-mediated DSBs repair

HDAC4 belongs to class IIa histone deacetylases, enzymes that possess poor catalytic activity and frequently interact with class I HDACs. Recent studies of my research group have shown that HDAC4 depletion triggers senescence and this process is associated with the accumulation of DNA damage. In particular, HDAC4 knock-down is associated with a defect in DNA repair by homologous recombination (HR). The aim of my PhD project is to investigate the epigenetic mechanisms that control genome stability maintenance, to pinpoint key druggable genome caretaker enzymes and to investigate their role in cellular transformation and senescence. For this work, we are studying HR impairment in different cellular models, including the induction of the endonuclease I-PpoI, and we are investigating the role of HDAC4 in this process. With different techniques, including in-vitro assays, we are examining the epigenetics modifications and HDAC4 partners involved.