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Nucleic Acids Research Advance Access published online on October 12, 2006
Nucleic Acids Research, doi:10.1093/nar/gkl705
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© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Nucleic Acid Enzymes

ATM mediates oxidative stress-induced dephosphorylation of DNA ligase III{alpha}

Zhiwan Dong and Alan E. Tomkinson1,*

Molecular and Cell Biology Graduate Program Baltimore, MD 21201-1509, USA 1 Radiation Oncology Research Laboratory, Department of Radiation Oncology and Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine Baltimore, MD 21201-1509, USA

*To whom correspondence should be addressed. Radiation Oncology Research Laboratory, Department of Radiation Oncology, and Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, 655 W. Baltimore St., Baltimore, MD 21201-1509, USA. Tel: +1 410 706 2365; Fax: +1 410 706 3000; Email: atomkinson{at}som.umaryland.edu

Received May 22, 2006. Revised September 8, 2006. Accepted September 12, 2006.

Among the three mammalian genes encoding DNA ligases, only the LIG3 gene does not have a homolog in lower eukaryotes. In somatic mammalian cells, the nuclear form of DNA ligase III{alpha} forms a stable complex with the DNA repair protein XRCC1 that is also found only in higher eukaryotes. Recent studies have shown that XRCC1 participates in S phase-specific DNA repair pathways independently of DNA ligase III{alpha} and is constitutively phosphorylated by casein kinase II. In this study we demonstrate that DNA ligase III{alpha}, unlike XRCC1, is phosphorylated in a cell cycle-dependent manner. Specifically, DNA ligase III{alpha} is phosphorylated on Ser123 by the cell division cycle kinase Cdk2 beginning early in S phase and continuing into M phase. Interestingly, treatment of S phase cells with agents that cause oxygen free radicals induces the dephosphorylation of DNA ligase III{alpha}. This oxidative stress-induced dephosphorylation of DNA ligase III{alpha} is dependent upon the ATM (ataxia-telangiectasia mutated) kinase and appears to involve inhibition of Cdk2 and probably activation of a phosphatase.


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