Finally, we show that the DNA breakage in replicating cells and apoptosis observed in WS are not enhanced by concomitant knock down of MRE11 by RNAi, indicating that WRN and MRE11 complex act in a common pathway.
However, recent emerging evidence suggests that one candidate for a sensor of replication stress is ATR and that, together with a member of RecQ family helicases, Werner syndrome protein (WRN) and MRE11 complex, can collaborate to promote the restarting of DNA synthesis through the resolution of stalled replication forks.