Origin of endogenous replicative stress, and consequences of RH defect on mitotic segregation:
Given its role in restarting the blocked replication forks, the RH defect thus makes it possible to reveal the endogenous stress. This axis provides on the one hand to identify the mechanisms responsible for the slowing down of the replication forks in the rh- cells (thus the original endogenous stress), on the other hand to analyse the consequences on the G2 phase of the defect of RH, leading to chaotic chromosomal segregations in mitosis.
In addition, we have developed a postnatal conditional inactivation of HR mouse model. The in vivo consequences of the invalidation of HR will therefore be analysed.