In a recent issue of DNA Repair [7 (2008) 1776–1786], Julia Sidorova reviews the role of WRN in preserving DNA integrity during replication and propose that WRN can function in coordinating replication fork progression with replication stress-induced fork remodeling. She further discusses damage tolerance pathways, redundancy, and cooperation with other RecQ helicases.
Fig. 3. Possible scenarios of WRN function in coordinating fork progression with damage repair via control over daughter/daughter duplex expansion and/or half-life. (A) An unproductive daughter/daughter duplex with the 3′ overhang is unwound to redirect damage bypass towards translesion synthesis (TLS). (B) An extension of a daughter/daughter duplex leads to exposure of ssDNA regions of mother strands (for simplicity, only one of the strands is shown coated with RPA). Accumulation of RPA stimulates helicase activity of WRN to limit propagation of daughter/daughter duplex and restore an original fork conformation. (C) Lagging strand synthesis in the presence of a daughter/daughter duplex can lead to formation of long flaps. WRN can prevent their formation by limiting half-life of a daughter/daughter duplex, or stimulate FEN-1 to cleave such flaps once they are formed.
DRUSE 
