Editorial: Protecting the code: DNA double-strand break repair pathway choice
Frontiers in Genetics, vol. 13, pp. 993889
Abstract
Editorial on the Research Topic Protecting the code: DNA double-strand break repair pathway choiceThe genetic information in our cells is constantly challenged by several sources that can cause DNA damage.Amongst the various lesions that can occur in the genome, DNA double-strand breaks (DSBs) are considered the most dangerous (Scully et al., 2019).Cells combat DSBs by activation of the DNA damage response (DDR), a complex evolutionary conserved cellular network that senses, signals and repairs DNA breaks, while coordinating DNA repair with chromatin regulation, gene expression, and cell cycle progression (Ciccia and Elledge, 2010).Defects in the DDR can lead to devastating diseases such as immune disorders and cancer (Jackson and Bartek, 2009).In addition, the targeted generation of DSBs can be exploited for CRISPR-mediated genome editing and gene therapy (Yeh et al., 2019;Nambiar et al., 2022).DSB repair is, therefore, one of the most critical tasks a cell must pursue to maintain genome integrity, and malfunction of this process has important clinical implications.This Research Topic is focused on Protecting the code: DNA double-strand break repair pathway choice and features 18 articles that reflect the complexity of cellular processes that determine DNA repair pathway choice.It consists of topical reviews as well as original research and methods articles focusing on key DNA repair mechanisms, including the main DSB repair pathways non-homologous end-joining (NHEJ) and homologous recombination (HR), and on techniques to study these pathways and elucidate their relevance for human health and disease.DSB repair pathway choice relies on multiple regulatory layers that can respond to environmental and cell-intrinsic cues (Chapman et al., 2012;Krenning et al., 2019).Amongst the latter are non-B DNA structures, which are formed at particular sequences
Authors 5
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Centre National de la Recherche Scientifique · Université Paris Sciences et Lettres · Leiden University Medical Center · Institut Curie
Affiliation as printed
Department of Human Genetics, Leiden University Medical Center, Leiden, Netherlands
Institut Curie, PSL University, CNRS, Orsay, France
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Leiden University Medical Center · Oncode Institute
Affiliation as printed
Department of Human Genetics, Leiden University Medical Center, Leiden, Netherlands
Oncode Institute, Utrecht, Netherlands
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Affiliation as printed
Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT, United States
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Affiliation as printed
Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO, United States
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Matthias Altmeyer corresponding
Affiliation as printed
Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland
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