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Nucleic Acids Research, 2003, Vol. 31, No. 3 1013-1023
© 2003 Oxford University Press

Genome instability in rad54 mutants of Saccharomyces cerevisiae

Jacqueline Schmuckli-Maurer, Michael Rolfsmeier1, Ho Nguyen1 and Wolf-Dietrich Heyer*,1,2

Division of Biological Sciences, 1 Section of Microbiology and 2 Section of Molecular and Cellular Biology and Center for Genetics and Development, University of California, Davis, Davis, CA 95616-8665, USA

*To whom correspondence should be addressed. Tel: +1 530 752 3001; Fax: +1 530 752 3011; Email: wdheyer{at}ucdavis.edu
Present address:
Jacqueline Schmuckli-Maurer, Institute of Animal Pathology, University of Bern, CH-3010 Bern, Switzerland

The RAD54 gene of Saccharomyces cerevisiae encodes a conserved dsDNA-dependent ATPase of the Swi2/Snf2 family with a specialized function during recombinational DNA repair. Here we analyzed the consequences of the loss of Rad54 function in vegetative (mitotic) cells. Mutants in RAD54 exhibited drastically reduced rates of spontaneous intragenic recombination but were proficient for spontaneous intergenic recombinant formation. The intergenic recombinants likely arose by a RAD54-independent pathway of break-induced replication. Significantly increased rates of spontaneous chromosome loss for diploid rad54/rad54 cells were identified in several independent assays. Inter estingly, the increase in chromosome loss appeared to depend on the presence of a homolog. In addition, the rate of complex genetic events involving chromosome loss were drastically increased in diploid rad54/rad54 cells. Together, these data suggest a role for Rad54 protein in the repair of spontaneous damage, where in the absence of Rad54 protein, homologous recombination is initiated but not properly terminated, leading to misrepair and chromosome loss.


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