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Complementation between polymerase- and exonuclease-deficient mitochondrial DNA polymerase mutants in genomically engineered flies.

Abstract：

:Replication errors are the main cause of mitochondrial DNA (mtDNA) mutations and a compelling approach to decrease mutation levels would therefore be to increase the fidelity of the catalytic subunit (POLγA) of the mtDNA polymerase. Here we genomically engineer the tamas locus, encoding fly POLγA, and introduce alleles expressing exonuclease- (exo(-)) and polymerase-deficient (pol(-)) POLγA versions. The exo(-) mutant leads to accumulation of point mutations and linear deletions of mtDNA, whereas pol(-) mutants cause mtDNA depletion. The mutant tamas alleles are developmentally lethal but can complement each other in trans resulting in viable flies with clonally expanded mtDNA mutations. Reconstitution of human mtDNA replication in vitro confirms that replication is a highly dynamic process where POLγA goes on and off the template to allow complementation during proofreading and elongation. The created fly models are valuable tools to study germ line transmission of mtDNA and the pathophysiology of POLγA mutation disease.

journal_name

Nat Commun

journal_title

Nature communications

authors

Bratic A,Kauppila TE,Macao B,Grönke S,Siibak T,Stewart JB,Baggio F,Dols J,Partridge L,Falkenberg M,Wredenberg A,Larsson NG

doi

10.1038/ncomms9808

subject

Has Abstract

pub_date

2015-11-10 00:00:00

pages

8808

issn

2041-1723

pii

ncomms9808

journal_volume

6

pub_type

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