Table 1.
Summary of factors that may promote fork regression
| Factor | Organism | Properties |
|---|---|---|
| DNA supercoiling | All | Non-enzymatic |
| RecG | E. coli | Superfamily 2 helicase, highly conserved in bacteria but no obvious (nuclear-encoded) eukaryotic homologues |
| RuvAB | E. coli | Inefficient initiation of fork regression but could promote branch migration of Holliday junctions formed by regression |
| RecQ homologues | H. sapiens | Highly conserved group of Superfamily 2 helicases. Not all RecQ-type helicases possess regression activity |
| UvsW | T4 bacteriophage | Superfamily 2 helicase, bears functional (but not structural) similarity to RecG |
| Rad5 | S. cerevisiae | Superfamily 2 DNA translocase but no detectable helicase activity |
| FANCM/Fml1 | H. sapiens/S. pombe | Superfamily 2 helicases. FANCM also contains an endonuclease domain |
| Hjm/Hel308 | S. tokodai | Superfamily 2 helicase |
| Strand exchange proteins | E. coli/T4 bacteriophage/H. sapiens | Ubiquitous. Initial binding requires ssDNA, implying regression by these enzymes may be fork structure-specific |
With the exception of RuvAB all helicases/translocases currently suspected of catalysing regression are Superfamily 2 motors. Whether this reflects specific properties of Superfamily 2 motors that are needed for efficient fork regression is unknown.