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Replication Stress: A Lifetime of Epigenetic Change

Laboratory for Receptor Biology and Gene Expression, National Cancer Institute, NIH, 41 Library Drive, Bethesda, MD 20892, USA
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Academic Editor: Jessica Tyler
Genes 2015, 6(3), 858-877; https://doi.org/10.3390/genes6030858
Received: 29 June 2015 / Revised: 4 September 2015 / Accepted: 8 September 2015 / Published: 11 September 2015
(This article belongs to the Special Issue Chromatin Dynamics)
DNA replication is essential for cell division. Challenges to the progression of DNA polymerase can result in replication stress, promoting the stalling and ultimately collapse of replication forks. The latter involves the formation of DNA double-strand breaks (DSBs) and has been linked to both genome instability and irreversible cell cycle arrest (senescence). Recent technological advances have elucidated many of the factors that contribute to the sensing and repair of stalled or broken replication forks. In addition to bona fide repair factors, these efforts highlight a range of chromatin-associated changes at and near sites of replication stress, suggesting defects in epigenome maintenance as a potential outcome of aberrant DNA replication. Here, we will summarize recent insight into replication stress-induced chromatin-reorganization and will speculate on possible adverse effects for gene expression, nuclear integrity and, ultimately, cell function. View Full-Text
Keywords: replication stress; DNA repair; chromatin; histones; senescence replication stress; DNA repair; chromatin; histones; senescence
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Khurana, S.; Oberdoerffer, P. Replication Stress: A Lifetime of Epigenetic Change. Genes 2015, 6, 858-877.

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