한빛사논문
Youngkyu Jeon1,4, Yilin Lu1,10, Margherita Maria Ferrari2,5,10, Tejasvi Channagiri2,10, Penghao Xu1,10, Chance Meers1,6, Yiqi Zhang1,7,8, Sathya Balachander1,9, Vivian S. Park3, Stefania Marsili1, Zachary F. Pursell3, Nataša Jonoska2 & Francesca Storici1
1School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA, USA.
2Department of Mathematics and Statistics, University of South Florida, Tampa, FL, USA.
3Department of Biochemistry and Molecular Biology, Tulane Cancer Center, Tulane University of Medicine, New Orleans, LA, USA.
4Present address: Molecular Targets Program, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH), Fredrick, MD, USA.
5Present address: Department of Mathematics, University of Manitoba, Winnipeg, MB, Canada.
6Present address: Columbia University Irving Medical Center, New York, NY, USA.
7Present address: Program for Lung and Vascular Biology, Section for Injury Repair and Regeneration Research, Stanley Manne Children’s Research Institute, Ann & Robert H. Lurie Children’s Hospital of Chicago, Chicago, IL, USA.
8Present address: Department of Pediatrics, Division of Critical Care, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
9Present address: Emory University, Atlanta, GA, USA.
10These authors contributed equally: Yilin Lu, Margherita Maria Ferrari, Tejasvi Channagiri, Penghao Xu.
Corresponding authors
Correspondence to Nataša Jonoska or Francesca Storici.
Abstract
Double-strand breaks (DSBs) in DNA are challenging to repair. Cells employ at least three DSB-repair mechanisms, with a preference for non-homologous end joining (NHEJ) over homologous recombination (HR) and microhomology-mediated end joining (MMEJ). While most eukaryotic DNA is transcribed into RNA, providing complementary genetic information, much remains unknown about the direct impact of RNA on DSB-repair outcomes and its role in DSB-repair via end joining. Here, we show that both sense and antisense-transcript RNAs impact DSB repair in a sequence-specific manner in wild-type human and yeast cells. Depending on its sequence complementarity with the broken DNA ends, a transcript RNA can promote repair of a DSB or a double-strand gap in its DNA gene via NHEJ or MMEJ, independently from DNA synthesis. The results demonstrate a role of transcript RNA in directing the way DSBs are repaired in DNA, suggesting that RNA may directly modulate genome stability and evolution.
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