Skip to main content
. Author manuscript; available in PMC: 2009 Nov 1.
Published in final edited form as: DNA Repair (Amst). 2008 Sep 6;7(11):1776–1786. doi: 10.1016/j.dnarep.2008.07.017

Figure 3. Possible scenarios of WRN function in coordinating fork progression with damage repair via control over daughter/daughter duplex expansion and/or half-life.

Figure 3

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.