Figure 9.—

A model for the genetic interaction between Pif1 and Sgs1–Top3. Pif1 interacts with the Sgs1–Top3 pathway downstream of homologous recombination. A concerted Sgs1–Top3 activity is proposed to be one means of resolving recombination intermediates at the end of DNA replication, such as the double Holliday junction that is pictured (Heyer et al. 2003). In this Sgs1–Top3 resolvase model, Sgs1 molecules act on opposing DNA strands to convergently branch migrate the Holliday junctions, forming a hemicatenated strand interlink that is resolved by Top3 (middle). In the absence of Top3, the Sgs1-created substrate persists, is not efficiently resolved by other pathways, and is toxic to the cell as evidenced by the myriad defects of top3 mutants (shaded box). In the absence of Sgs1 (sgs1 or sgs1 top3 strains), this toxic substrate is never created, leaving the recombination intermediate accessible to alternative pathways (white box). Our results demonstrate that Pif1 helicase activity is required to counteract Sgs1 helicase activity that has become uncoupled from Top3. Our data suggest that Pif1 either reverses or prevents formation of this detrimental Sgs1-created DNA structure.