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Published online 3 February 2004

Nucleic Acids Research, 2004, Vol. 32, No. 2 767-775
© 2004 Oxford University Press

Involvement of Hus1 in the chain elongation step of DNA replication after exposure to camptothecin or ionizing radiation

Xiang Wang, Jun Guan, Baocheng Hu, Robert S. Weiss1, George Iliakis2 and Ya Wang*

Department of Radiation Oncology, Kimmel Cancer Center of Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA, 1 Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853, USA and 2 Institute of Medical Radiation Biology, University of Duisburg-Essen Medical School, 45122 Essen, Germany

*To whom correspondence should be addressed. Tel: +1 215 955 2045; Fax: +1 215 955 2052; Email: ya.wang{at}mail.tju.edu
Present addresses:
Jun Guan, Department of Radiation Oncology, University of Pennsylvania, Philadelphia, PA 19104, USA
Baocheng Hu, Beijing Institute of Biotechnology, Beijing 100850, China
The authors wish it to be known that, in their opinion, the first three authors should be regarded as joint First Authors

DNA damage-induced S phase (S) checkpoint includes inhibition of both replicon initiation and chain elongation. The precise mechanism for controlling the two processes remains unclear. In this study, we showed that Hus1-deficient mouse cells had an impaired S checkpoint after exposure to DNA strand break-inducing agents such as camptothecin (CPT) (>=1.0 µM), or ionizing radiation (IR) (>=15 Gy). The Hus1-dependent S checkpoint contributes to cell resistance to CPT. This impaired S checkpoint induced by CPT or IR in Hus1-deficient cells reflected mainly the chain elongation step of DNA replication and was correlated with the reduction of dissociation of PCNA from DNA replication foci. Although Hus1 is required for Rad9 phosphorylation following exposure of cells to CPT or IR, Hus1-deficient cells showed normal activation of ATR/CHK1 and ATM kinases at doses where the checkpoint defects were manifested, suggesting that Hus1 is not a component of the sensor system for activating these pathways in S checkpoint induced by CPT or IR.


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