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Replication Stress, Genomic Instability, and Replication Timing: A Complex Relationship
Article

Low Replicative Stress Triggers Cell-Type Specific Inheritable Advanced Replication Timing

1
Centre de Recherches en Cancérologie de Toulouse (CRCT), UMR1037 Inserm, University Paul Sabatier III, ERL5294 CNRS, 2 Avenue Hubert Curien, 31037 Toulouse, France
2
Université de Paris, CNRS, Institut Jacques Monod, DNA Replication Pathologies Team, F-75006 Paris, France
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
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editors: Jihane Basbous, Cyril Ribeyre and Takahiko Shimizu
Int. J. Mol. Sci. 2021, 22(9), 4959; https://doi.org/10.3390/ijms22094959
Received: 31 March 2021 / Revised: 30 April 2021 / Accepted: 2 May 2021 / Published: 7 May 2021
(This article belongs to the Special Issue DNA Replication Stress and Chromosomal Instability)
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 also generate RT advances that are still uncharacterized. In order to characterize these advanced initiation events, we monitored the whole genome RT from six independent human cell lines treated with low doses of aphidicolin. We report that RT advances are cell-type-specific and involve large heterochromatin domains. Importantly, we found that some major late to early RT advances can be inherited by the unstressed next-cellular generation, which is a unique process that correlates with enhanced chromatin accessibility, as well as modified replication origin landscape and gene expression in daughter cells. Collectively, this work highlights how low replication stress may impact cellular identity by RT advances events at a subset of chromosomal domains. View Full-Text
Keywords: DNA replication stress; DNA replication timing; chromatin accessibility; DNA damage DNA replication stress; DNA replication timing; chromatin accessibility; DNA damage
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MDPI and ACS Style

Courtot, L.; Bournique, E.; Maric, C.; Guitton-Sert, L.; Madrid-Mencía, M.; Pancaldi, V.; Cadoret, J.-C.; Hoffmann, J.-S.; Bergoglio, V. Low Replicative Stress Triggers Cell-Type Specific Inheritable Advanced Replication Timing. Int. J. Mol. Sci. 2021, 22, 4959. https://doi.org/10.3390/ijms22094959

AMA Style

Courtot L, Bournique E, Maric C, Guitton-Sert L, Madrid-Mencía M, Pancaldi V, Cadoret J-C, Hoffmann J-S, Bergoglio V. Low Replicative Stress Triggers Cell-Type Specific Inheritable Advanced Replication Timing. International Journal of Molecular Sciences. 2021; 22(9):4959. https://doi.org/10.3390/ijms22094959

Chicago/Turabian Style

Courtot, Lilas, Elodie Bournique, Chrystelle Maric, Laure Guitton-Sert, Miguel Madrid-Mencía, Vera Pancaldi, Jean-Charles Cadoret, Jean-Sébastien Hoffmann, and Valérie Bergoglio. 2021. "Low Replicative Stress Triggers Cell-Type Specific Inheritable Advanced Replication Timing" International Journal of Molecular Sciences 22, no. 9: 4959. https://doi.org/10.3390/ijms22094959

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