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Reference: Pogorzala LA, et al. (2009) Evidence that msh1p plays multiple roles in mitochondrial base excision repair. Genetics 182(3):699-709

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Abstract

Mitochondrial DNA is thought to be especially prone to oxidative damage by ROS generated through electron transport during cellular respiration. This damage is primarily mitigated by the base excision repair (BER) pathway, one of the few DNA repair pathways with confirmed activity on mitochondrial DNA. Through genetic epistasis analysis in the yeast Saccharomyces cerevisiae, we examined the genetic interaction between each of the BER proteins previously shown to localize to the mitochondria. In addition, we describe a series of genetic interactions between BER components and the MutS homolog MSH1, a respiration-essential gene. We show that in addition to their variable effects on mitochondrial function, mutant msh1 alleles conferring partial function interact genetically at different points in mitochondrial BER. In addition to this separation of function, we also found that the role of Msh1p in BER is unlikely to be involved in the avoidance of large-scale deletions and rearrangements.

Reference Type
Journal Article
Authors
Pogorzala LA, Mookerjee S, Sia EA
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