Journal
CELLS
Volume 9, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/cells9071657
Keywords
alt-EJ; polymerase theta; microhomology-mediated end joining; chromosome rearrangements; resection
Categories
Funding
- National Science Foundation [MCB1716039]
- National Institutes of Health [P01GM10547, R01GM125827]
Ask authors/readers for more resources
Double-strand breaks are one of the most deleterious DNA lesions. Their repair via error-prone mechanisms can promote mutagenesis, loss of genetic information, and deregulation of the genome. These detrimental outcomes are significant drivers of human diseases, including many cancers. Mutagenic double-strand break repair also facilitates heritable genetic changes that drive organismal adaptation and evolution. In this review, we discuss the mechanisms of various error-prone DNA double-strand break repair processes and the cellular conditions that regulate them, with a focus on alternative end joining. We provide examples that illustrate how mutagenic double-strand break repair drives genome diversity and evolution. Finally, we discuss how error-prone break repair can be crucial to the induction and progression of diseases such as cancer.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available