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Originally published as Genetics Published Articles Ahead of Print on March 17, 2006.

Genetics, Vol. 173, 697-708, June 2006, Copyright © 2006
doi:10.1534/genetics.106.056879

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Homologous Recombination Is Required for Genome Stability in the Absence of DOG-1 in Caenorhabditis elegans

Jillian L. Youds, Nigel J. O'Neil and Ann M. Rose1

Department of Medical Genetics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada

1 Corresponding author: Department of Medical Genetics, Faculty of Medicine, University of British Columbia, NCE Bldg. Room 421–2125 East Mall, Vancouver, BC V6T 1Z3, Canada.
E-mail: arose{at}gene.nce.ubc.ca

In C. elegans, DOG-1 prevents deletions that initiate in polyG/polyC tracts (G/C tracts), most likely by unwinding secondary structures that can form in G/C tracts during lagging-strand DNA synthesis. We have used the dog-1 mutant to assay the in vivo contribution of various repair genes to the maintenance of G/C tracts. Here we show that DOG-1 and the BLM ortholog, HIM-6, act synergistically during replication; simultaneous loss of function of both genes results in replicative stress and an increase in the formation of small deletions that initiate in G/C tracts. Similarly, we demonstrate that the C. elegans orthologs of the homologous recombination repair genes BARD1, RAD51, and XPF and the trans-lesion synthesis polymerases pol{eta} and pol{kappa} contribute to the prevention of deletions in dog-1 mutants. Finally, we provide evidence that the small deletions generated in the dog-1 background are not formed through homologous recombination, nucleotide excision repair, or nonhomologous end-joining mechanisms, but appear to result from a mutagenic repair mechanism acting at G/C tracts. Our data support the hypothesis that absence of DOG-1 leads to replication fork stalling that can be repaired by deletion-free or deletion-prone mechanisms.




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