Another approach studies the mechanisms of carcinogen-induced genetic recombination using human cells containing two defective copies of a selectable gene, stably integrated into a chromosome. Only cells that combine the first part of one gene and the last part of the other gene can survive selection. This system allows us to quantify the frequency of recombination caused by various carcinogenic agents and to determine the nature of the recombination event. We also study the role of DNA repair in this recombination. The research is carried out by a staff of 15-20, composed of postdoctoral research associates, graduate students, and research assistants from the U.S. or abroad.
Funding comes mainly from federal grants for research and training.
Students interested in carcinogenesis, mutagenesis, and molecular and cellular biology are encouraged to discuss their interests with one of the directors and carry out a rotation in the laboratory to become personally acquainted with the research being conducted. V.M. The function of human homolog of Saccharomyces cerevisiae REV1 is required for mutagenesis induced by UV light. Qing, J., Wei, D., Maher, V.M., McCormick, J.J. Cloning and characterization of a novel gene encoding a putative transmembrane protein with altered expression in some human transformed and tumor-derived cell lines. McGregor, W.G., Wei, D., Maher, V.M., McCormick, J.J. Abnormal, error-prone bypass of photoproducts by xeroderma pigmentosum variant cell extracts results in extreme strand stand bias for the kinds of mutations induced by UV light. A human homolog of the Saccharomyces cerevisiae REV3 gene, which encodes the catalytic subunit of DNA polymerase zeta.