Journal
GENETICS
Volume 194, Issue 2, Pages 519-522Publisher
GENETICS SOCIETY AMERICA
DOI: 10.1534/genetics.113.150920
Keywords
-
Categories
Funding
- NIEHS
- National Institutes of Health [ES-065078]
Ask authors/readers for more resources
The importance of mitochondrial DNA (mtDNA) deletions in the progeroid phenotype of exonuclease-deficient DNA polymerase gamma mice has been intensely debated. We show that disruption of Mip1 exonuclease activity increases mtDNA deletions 160-fold, whereas disease-associated polymerase variants were mostly unaffected, suggesting that exonuclease activity is vital to avoid deletions during mtDNA replication.
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