Zim17/Tim15 links mitochondrial iron-sulfur cluster biosynthesis to nuclear genome stability.

ABSTRACT: Genomic instability is related to a wide-range of human diseases. Here, we show that mitochondrial iron-sulfur cluster biosynthesis is important for the maintenance of nuclear genome stability in Saccharomyces cerevisiae. Cells lacking the mitochondrial chaperone Zim17 (Tim15/Hep1), a component of the iron-sulfur biosynthesis machinery, have limited respiration activity, mimic the metabolic response to iron starvation and suffer a dramatic increase in nuclear genome recombination. Increased oxidative damage or deficient DNA repair do not account for the observed genomic hyperrecombination. Impaired cell-cycle progression and genetic interactions of ZIM17 with components of the RFC-like complex involved in mitotic checkpoints indicate that replicative stress causes hyperrecombination in zim

SUBMITTER: Diaz de la Loza Mdel C 

PROVIDER: S-EPMC3152343 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature