In eukaryotes, replication does not proceed normally in the absence of RecQ proteins, which also function in aging, silencing, recombination and DNA repair.
[citation needed] RecQ family members share three regions of conserved protein sequence referred to as the: The removal of the N-terminal residues (Helicase and, RecQ-Ct domains) impairs both helicase and ATPase activity but has no effect on the binding ability of RecQ implying that the N-terminus functions as the catalytic end.
The emerging picture clearly is that RecQ helicases in concert with Top 3 are involved in maintaining genomic stability and integrity by controlling recombination events, and repairing DNA damage in the G2-phase of the cell cycle.
The process likely involves the helicase and exonuclease activities of WRN that operate together with DNA polymerase beta in long patch base excision repair.
[9] WRN was found to have a specific role in preventing or repairing DNA damages resulting from chronic oxidative stress, particularly in slowly replicating cells.
The budding yeast Saccharomyces cerevisiae encodes an ortholog of the Bloom syndrome (BLM) protein that is designated Sgs1 (Small growth suppressor 1).
[12] During normal meiosis Sgs1(BLM) is responsible for directing recombination towards the alternate formation of either early non-crossovers or Holliday junction joint molecules, the latter being subsequently resolved as crossovers.
[15] RECQL4 has a crucial role in DNA end resection that is the initial step required for homologous recombination (HR)-dependent double-strand break repair.