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Carcinogenesis Advance Access published online on January 23, 2004
Carcinogenesis, doi:10.1093/carcin/bgh085
© 2004 by Oxford University Press
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© 2004 Oxford University Press

CARCINOGENESIS

UV radiation-induced XPC translocation within chromatin is mediated by damaged-DNA binding protein, DDB2

Qi-En Wang 1, Qianzheng Zhu 1, Gulzar Wani 1, Jianming Chen 1, and Altaf A. Wani 2*

1 Department of Radiology, The Ohio State University, Columbus, OH 43210
2 Department of Radiology, The Ohio State University, Columbus, OH 43210; Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, OH 43210; James Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH 43210

* Corresponding author. E-mail: wani.2{at}osu.edu.

Received 8 September 2003 ; revised 6 January 2004 ; accepted 10 January 2004

Abstract

The tumor suppressor p53 protein has been established as an important factor in modulating the efficiency of global genomic repair. Our recent repair studies in human cells reported that p53 regulates the recruitment of XPC and TFIIH proteins to specific DNA damage sites. Here, we have examined the influence of p53 and DDB2 proteins on the distribution of XPC within damaged chromatin in vivo and the recruitment of XPC to DNA damage sites in situ. The results show that UV irradiation causes the translocation of XPC from a loosely bound form into a tight association with chromatin in vivo. The UV radiation-induced redistribution of XPC was equally compromised in p53-deficient, as well as DDB2-deficient, human cells. Similarly, rapid recruitment of XPC to DNA damage in situ was also impaired in both cell lines. Ectopic expression of DDB2 in p53-deficient cells overcame the requirement of p53 function for UVinduced translocation of XPC in vivo. Restoration of DDB2 function also enhanced the recruitment of XPC to DNA damage sites in situ and increased the global repair of CPD from the genome. These results indicate that DDB2 is a key downstream factor of p53 for regulating the movement of XPC to DNA damage in irradiated cells.

UV radiation, DNA damage, DNA repair, p53, DDB2, XPC
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