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CRISPR-Cas immunity, DNA repair and genome stability

Cubbon, Andrew; Ivancic-Bace, Ivana; Bolt, Edward�L.

Authors

Andrew Cubbon

Ivana Ivancic-Bace

ED BOLT ED.BOLT@NOTTINGHAM.AC.UK
Professor of Molecular Biology



Abstract

© 2018 The Author(s). Co-opting of CRISPR-Cas ‘Interference’ reactions for editing the genomes of eukaryotic and prokaryotic cells has highlighted crucial support roles for DNA repair systems that strive to maintain genome stability. As front-runners in genome editing that targets DNA, the class 2 CRISPR-Cas enzymes Cas9 and Cas12a rely on repair of DNA double-strand breaks (DDSBs) by host DNA repair enzymes, using mechanisms that vary in how well they are understood. Data are emerging about the identities of DNA repair enzymes that support genome editing in human cells. At the same time, it is becoming apparent that CRISPR-Cas systems functioning in their native environment, bacteria or archaea, also need DNA repair enzymes. In this short review, we survey how DNA repair and CRISPR-Cas systems are intertwined. We consider how understanding DNA repair and CRISPR-Cas interference reactions in nature might help improve the efficacy of genome editing procedures that utilise homologous or analogous systems in human and other cells.

Citation

Cubbon, A., Ivancic-Bace, I., & Bolt, E. (2018). CRISPR-Cas immunity, DNA repair and genome stability. Bioscience Reports, 38(5), 1-10. https://doi.org/10.1042/bsr20180457

Journal Article Type Article
Acceptance Date Sep 10, 2018
Online Publication Date Sep 12, 2018
Publication Date Sep 21, 2018
Deposit Date Dec 6, 2018
Publicly Available Date Dec 7, 2018
Journal Bioscience Reports
Print ISSN 0144-8463
Electronic ISSN 1573-4935
Publisher Portland Press
Peer Reviewed Peer Reviewed
Volume 38
Issue 5
Article Number BSR20180457
Pages 1-10
DOI https://doi.org/10.1042/bsr20180457
Keywords Biophysics; Cell biology; Biochemistry; Molecular biology
Public URL https://nottingham-repository.worktribe.com/output/1380212
Publisher URL http://www.bioscirep.org/content/38/5/BSR20180457

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