A. Ishchenko participates in this study of the fate of the DNA-protein crosslinks generated by the activity of AP endonucleases using two in vitro models of APPXLs (AP-peptide cross-links).
In a collaborative effort, the Mazon/Le Cam team used Cryo-EM to reveal how Rap1 inhibits Ku’s NHEJ activity at telomeres.
Rap1 binds near DNA breaks, blocking Ku’s inward translocation without displacing it. The study uncovers how Ku switches from repair-promoting to protective roles at telomeres.
F. Rosselli’s team shows in this article how abnormal p21 expression in Fanconi anemia (FA) contributes to bone marrow failure and genetic instability.
This upregulation depends not only on p53 but also on MITF and its interaction with NPM1.
In FA cells, p21 accumulates on chromatin, binds PCNA, and prolongs S-phase, leading to replication stress.
Depleting p21 restores replication timing and reduces instability.
ROS levels in FA cells promote p21-PCNA association, further impairing DNA replication.
In this article, the Mazon’s team PhD student H. Dorison goes deeper in the understanding of the SUMO-mediated regulation of the resolvase Yen1 in mitotic cells.
Lead by the postdocs of Mazon’s team, I. Talhaoui and M. Bernal, the article describes the regulation of Yen1 resolvase protein pools to control mitotic crossove formation during DSB repair.