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doi:10.1534/genetics.106.056879
A more recent version of this article appeared on June 1, 2006.
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Homologous recombination is required for genome stability in absence of DOG-1 in Caenorhabditis elegans
Jillian L Youds 1, Nigel J O'Neil 1 and Ann M Rose 1*
1 Department of Medical Genetics, Faculty of Medicine, University of British Columbia
* To whom correspondence should be addressed. E-mail: arose{at}gene.nce.ubc.ca.
Submitted on February 8, 2006
Revised on March 14, 2006
Accepted on 14 March 2006
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 poleta and polkappa 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 non-homologous 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.
Key Words: Caenorhabditis elegans, DNA secondary structure, genome stability, recombinational repair, stalled replication fork
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