International Journal of Molecular Sciences Article Low Replicative Stress Triggers Cell-Type Specific Inheritable Advanced Replication Timing Lilas Courtot 1 , Elodie Bournique 1,†, Chrystelle Maric 2,† , Laure Guitton-Sert 1, Miguel Madrid-Mencía 1 , Vera Pancaldi 1,3 , Jean-Charles Cadoret 2,* , Jean-Sébastien Hoffmann 4,* and Valérie Bergoglio 1,* 1 Centre de Recherches en Cancérologie de Toulouse (CRCT), UMR1037 Inserm, University Paul Sabatier III, ERL5294 CNRS, 2 Avenue Hubert Curien, 31037 Toulouse, France;
[email protected] (L.C.);
[email protected] (E.B.);
[email protected] (L.G.-S.);
[email protected] (M.M.-M.);
[email protected] (V.P.) 2 Université de Paris, CNRS, Institut Jacques Monod, DNA Replication Pathologies Team, F-75006 Paris, France;
[email protected] 3 Barcelona Supercomputing Center, 08034 Barcelona, Spain 4 Laboratoire de pathologie, Laboratoire d’excellence Toulouse Cancer, Institut Universitaire du Cancer-Toulouse, Oncopole, 1 Avenue Irène-Joliot-Curie, CEDEX, 31059 Toulouse, France * Correspondence:
[email protected] (J.-C.C.);
[email protected] (J.-S.H.);
[email protected] (V.B.) † These authors contributed equally to this work. Abstract: DNA replication timing (RT), reflecting the temporal order of origin activation, is known as a robust and conserved cell-type specific process. Upon low replication stress, the slowing of replication forks induces well-documented RT delays associated to genetic instability, but it can Citation: Courtot, L.; Bournique, E.; also generate RT advances that are still uncharacterized. In order to characterize these advanced Maric, C.; Guitton-Sert, L.; initiation events, we monitored the whole genome RT from six independent human cell lines treated Madrid-Mencía, M.; Pancaldi, V.; Cadoret, J.-C.; Hoffmann, J.-S.; with low doses of aphidicolin.