Abstract:
:The importance of mitochondrial DNA (mtDNA) deletions in the progeroid phenotype of exonuclease-deficient DNA polymerase γ 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.
journal_name
Geneticsjournal_title
Geneticsauthors
Stumpf JD,Copeland WCdoi
10.1534/genetics.113.150920subject
Has Abstractpub_date
2013-06-01 00:00:00pages
519-22issue
2eissn
0016-6731issn
1943-2631pii
genetics.113.150920journal_volume
194pub_type
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