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Background  The presence of inverted repeats (IRs) in DNA poses an obstacle to the normal progression of the DNA replication machinery, because these sequences can form secondary structures ahead of the replication fork. A failure to process and to restart the stalled replication machinery can lead to the loss of genome integrity. Consistently, IRs have been found to be associated with a high level of genome rearrangements, including deletions, translocations, inversions, and a high rate of sister-chromatid exchange (SCE). The RecQ helicase Sgs1, in  Saccharomyces cerevisiae , is believed to act on stalled replication forks. To determine the role of Sgs1 when the replication machinery stalls at the secondary structure, we measured the rates of IR-associated and non-IR-associated spontaneous unequal SCE events in the  sgs1  mutant, and in strains bearing mutations in genes that are functionally related to  SGS1 .    Results  The rate of SCE in  sgs1  cells for both IR and non-IR-containing substrates was higher than the rate in the wild-type background. The  srs2  and  mus81  mutations had modest effects, compared to  sgs1 . The  exo1  mutation increased SCE rates for both substrates. The  sgs1 exo1  double mutant exhibited synergistic effects on spontaneous SCE. The IR-associated SCE events in  sgs1  cells were partially  MSH2 -dependent.    Conclusions  These results suggest that Sgs1 suppresses spontaneous unequal SCE, and  SGS1  and  EXO1  regulate spontaneous SCE by independent mechanisms. The mismatch repair proteins, in contradistinction to their roles in mutation avoidance, promote secondary structure-associated genetic instability.

bmc molecular biology

Effects of mutations in SGS1 and in genes functionally related to SGS1 on inverted repeat-stimulated spontaneous unequal sister-chromatid exchange in yeast