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	Proc. Natl. Acad. Sci. U.S.A. Jun (2007); 104(23):9747-52
Oxygen metabolism and reactive oxygen species cause chromosomal rearrangements and cell death-
Ragu S, Faye G, Iraqui I, Masurel-Heneman A, Kolodner RD, Huang ME
Centre National de la Recherche Scientifique, Unite Mixte de Recherche 2027, Institut Curie, Batiment 110, Centre Universitaire, 91405 Orsay, France-
Abstract: The absence of Tsa1, a key peroxiredoxin that functions to scavenge H-2-O-2- in Saccharomyces cerevisiae, causes the accumulation of a broad spectrum of mutations including gross chromosomal rearrangements -GCRs-- Deletion of TSA1 also causes synthetic lethality in combination with mutations in RAD6 and several key genes involved in DNA double-strand break repair- In the present study we investigated the causes of GCRs and cell death in these mutants- tsa1-associated GCRs were independent of the activity of the translesion DNA polymerases zeta, eta, and Rev1- Anaerobic growth reduced substantially GCR rates of WT and tsa1 mutants and restored the viability of tsa1 rad6, tsa1 rad51, and tsa1 mre11 double mutants- Anaerobic growth also reduced the GCR rate of rad27, pif1, and rad52 mutants, indicating a role of reactive oxygen species in GCR formation in these mutants- In addition, deletion of TSA1 or H-2-O-2- treatment of WT cells resulted in increased formation of Rad52 foci, sites of repair of multiple DNA lesions- H-2-O-2- treatment also induced the GCRs- Our results provide in vivo evidence that oxygen metabolism and reactive oxygen species are important sources of DNA damages that can lead to GCRs and lethal effects in S- cerevisiae-
[PUBMED: 17535927]

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Chris Stark, Bobby-Joe Breitkreutz, Teresa Reguly, Lorrie Boucher, Ashton Breitkreutz, Mike Tyers.
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