한빛사논문
- 조회165
Yang Liu 1,5,6, W. Taylor Cottle 1,6, Taekjip Ha 1,2,3,4
1Department of Biophysics and Biophysical Chemistry, Johns Hopkins University, Baltimore, MD, USA
2Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA
3Department of Biophysics, Johns Hopkins University, Baltimore, MD, USA
4Howard Hughes Medical Institute, Baltimore, MD, USA
5Present address: Department of Biochemistry, University of Utah, Salt Lake City, UT, USA
6These authors contributed equally
Correspondence: Taekjip Ha
Abstract
DNA double-strand breaks (DSBs) are one of the most genotoxic DNA lesions, driving a range of pathological defects from cancers to immunodeficiencies. To combat genomic instability caused by DSBs, evolution has outfitted cells with an intricate protein network dedicated to the rapid and accurate repair of these lesions. Pioneering studies have identified and characterized many crucial repair factors in this network, while the advent of genome manipulation tools like clustered regularly interspersed short palindromic repeats (CRISPR)-CRISPR-associated protein 9 (Cas9) has reinvigorated interest in DSB repair mechanisms. This review surveys the latest methodological advances and biological insights gained by utilizing Cas9 as a precise 'damage inducer' for the study of DSB repair. We highlight rapidly inducible Cas9 systems that enable synchronized and efficient break induction. When combined with sequencing and genome-specific imaging approaches, inducible Cas9 systems greatly expand our capability to spatiotemporally characterize cellular responses to DSB at specific genomic coordinates, providing mechanistic insights that were previously unobtainable.
논문정보
- Review Paper
- 2023년 03월 (BRIC 등록일 2023-06-09)
- 국외 연구진
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