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Journal of Virology, May 1999, p. 4299-4304, Vol. 73, No. 5
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Disruption of Nucleotide Excision Repair by the Human T-Cell Leukemia Virus Type 1 Tax Protein

Shyan-Yuan Kao and Susan J. Marriott*

Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030

Received 16 September 1998/Accepted 1 February 1999

The Tax protein of human T-cell leukemia virus type 1 (HTLV-1) is a transcriptional transactivator and viral oncogene. Since cellular transformation has been frequently linked to alterations in genome stability, we investigated the effect of Tax on nucleotide excision repair (NER), a prominent cellular DNA repair pathway. Cells expressing Tax exhibited a reduced capacity for NER as measured by unscheduled DNA synthesis and host cell reactivation assays. The cellular proliferating cell nuclear antigen (PCNA) gene product regulates DNA replication and repair pathways, including NER. Since Tax activates transcription of the PCNA promoter, we investigated whether this activity contributes to the reduction of NER. Tax increased endogenous PCNA protein expression, and analysis of Tax mutant proteins demonstrated that the reduction in NER correlated with Tax transactivation of PCNA gene expression. Direct overexpression of PCNA also reduced NER. We propose that overexpression of PCNA, and disruption of NER induced by Tax, predisposes cells to accumulate DNA damage and contributes to HTLV-1 transformation.

* Corresponding author. Mailing address: Baylor College of Medicine, Division of Molecular Virology, One Baylor Plaza, Houston, TX 77030. Phone: (713) 798-4440. Fax: (713) 798-3490. E-mail: susanm{at}bcm.tmc.edu.

Journal of Virology, May 1999, p. 4299-4304, Vol. 73, No. 5
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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