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. Author manuscript; available in PMC: 2007 Mar 19.
Published in final edited form as: Curr Genet. 2005 Nov 4;48(4):213–225. doi: 10.1007/s00294-005-0014-5

Fig. 7.

Fig. 7

Models of SGS1,MUS81, and RAD51 function. a RNH202 is shown mediating a repair pathway that runs parallel to three others. Pathway#1 is defined by MUS81 and is RAD51-independent. Pathway#2 is defined by SGS1 and RAD51. MUS81 may have a minor role downstream of RAD51 and is presented as pathway#3. b In this model, RNA primers are retained on an unknown fraction of Okazaki fragments. If the hybrid is long lived, it could become displaced by DNA polymerase and isomerize with the nascent DNA to produce a superfluous 3′-flap. This substrate could be cleaved by MUS81 endonuclease in a RAD51-independent pathway, allowing the hybrid to reform. Subsequently, the primer could be removed by a repair polymerase, in combination with Rad27 and/or Dna2. Alternatively, the 3′-end may be recombinogenic and feed into a RAD51-dependent pathway. The major pathway (#2), involves the formation of double Holliday junctions and resolution by SGS1-TOP3. A minor pathway (#3, in brackets) may involve RAD51-mediated strand invasion, partial extension, and strand displacement to produce a larger 3′-flap that is repaired by MUS81 and ultimately by RAD27 and/or DNA2.