Nature Communications (Sep 2019)
ARID1A promotes genomic stability through protecting telomere cohesion
- Bo Zhao,
- Jianhuang Lin,
- Lijie Rong,
- Shuai Wu,
- Zhong Deng,
- Nail Fatkhutdinov,
- Joseph Zundell,
- Takeshi Fukumoto,
- Qin Liu,
- Andrew Kossenkov,
- Stephanie Jean,
- Mark G. Cadungog,
- Mark E. Borowsky,
- Ronny Drapkin,
- Paul M. Lieberman,
- Cory T. Abate-Shen,
- Rugang Zhang
Affiliations
- Bo Zhao
- Gene Expression and Regulation Program, The Wistar Institute
- Jianhuang Lin
- Gene Expression and Regulation Program, The Wistar Institute
- Lijie Rong
- Department of Pharmacology, Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center
- Shuai Wu
- Gene Expression and Regulation Program, The Wistar Institute
- Zhong Deng
- Gene Expression and Regulation Program, The Wistar Institute
- Nail Fatkhutdinov
- Gene Expression and Regulation Program, The Wistar Institute
- Joseph Zundell
- Gene Expression and Regulation Program, The Wistar Institute
- Takeshi Fukumoto
- Gene Expression and Regulation Program, The Wistar Institute
- Qin Liu
- Molecular and Cellular Oncogenesis Program, The Wistar Institute
- Andrew Kossenkov
- Center for Systems and Computational Biology, The Wistar Institute
- Stephanie Jean
- Helen F. Graham Cancer Center & Research Institute
- Mark G. Cadungog
- Helen F. Graham Cancer Center & Research Institute
- Mark E. Borowsky
- Helen F. Graham Cancer Center & Research Institute
- Ronny Drapkin
- Department of Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania
- Paul M. Lieberman
- Gene Expression and Regulation Program, The Wistar Institute
- Cory T. Abate-Shen
- Department of Pharmacology, Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center
- Rugang Zhang
- Gene Expression and Regulation Program, The Wistar Institute
- DOI
- https://doi.org/10.1038/s41467-019-12037-4
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 13
Abstract
Cells with ARID1A mutations exhibit mitotic defects, yet show surprisingly low levels of copy number defects. Here, Zhao et al. resolve this issue by showing that ARID1A loss causes defects in telomere cohesion, which selects against gross alterations in copy number.
