FIG. 5.
Model for the suppression of homology-driven translocations in the absence of Sgs1 helicase. Replication stress as well as defects in DNA damage checkpoints, the DNA replication checkpoint, and chromatin assembly can lead to increased levels of HR-dependent translocations in sgs1Δ mutants, while lack of the checkpoint kinase Mec1 or Rad53 or a defective oxidative response preferentially leads to other GCR types, such as de novo telomere additions and translocations without homology at the breakpoint (see the text for details).