Abstract
Werner syndrome (WS) is a disorder with multiple features of premature aging. The responsible WRN gene encodes a protein possessing DNA helicase and exonuclease. To examine the differential function of helicase and exonuclease of WRN protein, we investigated cell cycle progression after treatment with hydroxyurea (HU) in a WS cell line (WS780) and a human cell line (293delta231) defected in a WRN exonuclease activity. The results indicated that WS780 cells were highly sensitive to HU treatment, showing a more delayed recovery from the DNA replication (S) arrest than a control GM638 cell line. In contrast, the WRN exonuclease defective cell line (293delta231) showed no difference in the recovery from the S arrest as compared with a control 293 cell line. The present results suggest that WRN protein play a role in the recovery from the S arrest although WRN exonuclease is not involved in this process. [J Radiat Res 44:410 (2003)]