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Boyer Center for Molecular Medicine [F. M. H., Y-H. C., S. M. W.] and Departments of Neurology [F. M. H.] and Genetics [Y-H. C., S. M. W.], Yale University School of Medicine, New Haven, Connecticut 06520; Department of Medical and Molecular Genetics, Hospital for Sick Children, University of Toronto, Toronto, Ontario, M5G 1X8 Canada [M. S. M.]; and Department of Pathology, University of Washington, Seattle, Washington 98195 [J. O.]
WRN encodes a RecQ helicase, which is mutated in Werner syndrome. Werner syndrome is a genetic condition of young adults characterized by premature aging, limited replicative capacity of cells in vitro, and increased cancer risk. Telomerase is a reverse transcriptase that extends the G-rich strand of telomeric DNA. Primary cells in vitro typically lack telomerase activity and undergo senescence, whereas telomerase is reactivated in many, but not all, tumors. The roles of the two genes are not known to be related. Here we report the development of an effective colony-forming assay in which a SV40-transformed Werner fibroblast cell line is 6–18-fold more sensitive to 4-nitroquinoline 1-oxide than SV40-transformed normal cell lines. The sensitivity can be partially reversed by transfecting a normal WRN gene but not a mutated WRN gene into the cells. Curiously, the sensitivity can be reversed equally well by transfecting a telomerase gene (TERT) into the cells. These data indicate the possibility of an interdependent function of these two genes.
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R. M. Brosh Jr., A. Majumdar, S. Desai, I. D. Hickson, V. A. Bohr, and M. M. Seidman Unwinding of a DNA Triple Helix by the Werner and Bloom Syndrome Helicases J. Biol. Chem., January 26, 2001; 276(5): 3024 - 3030. [Abstract] [Full Text] [PDF]
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P. L. Opresko, J.-P. Laine, R. M. Brosh Jr., M. M. Seidman, and V. A. Bohr Coordinate Action of the Helicase and 3' to 5' Exonuclease of Werner Syndrome Protein J. Biol. Chem., November 21, 2001; 276(48): 44677 - 44687. [Abstract] [Full Text] [PDF]
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