Doug Bishop, Ph.D.

APPOINTMENTS

  • Professor, Department of Radiation and Cellular Oncology, Department of Molecular Genetics and Cell Biology, Committee on Cancer Biology, Committee on Genetics

EDUCATION

Ph.D., Harvard, 1988

CONTACT INFORMATION

The University of Chicago
CLSC 821B
920 East 58th Street
Chicago, Illinois 60637

Lab: CLSC 817

dbishop@midway.uchicago.edu

Phone:  (773) 702-9211

Lab:       (773) 702-3088

Lab Website

RESEARCH SUMMARY

Responses to DNA Damage in S. cerevisiae; Recombinational Repair and Cell Cycle Regulation

Homologous recombination of DNA repairs DNA damage and also creates the physical connections between chromosomes needed for reductional chromosome segregation during meiosis. We study two recombination proteins, Dmc1 and Rad51 that are related to the bacterial repair protein, RecA. The mechanisms of recombinational repair of damage induced double strand breaks in DNA (DSBs) and the mechanism of meiotic recombination are very closely related in terms of the DNA intermediates that form; DSBs are normal intermediates in most or all meiotic recombination. There are, however critical differences in how meiotic recombination is regulated as compared to mitotic recombinational repair. Our research is directed at understanding how Dmc1's function is specialized for meiosis, how the functions of Rad51 and Dmc1 differ, how the two proteins interact with one another during meiosis, and how the two proteins interact with components of the synaptonemal complex. Our studies have shown that while the functions of Rad51 and Dmc1 overlap, they are also functionally distinct.

Using biochemical techniques we recently showed that, like yeast Rad51 protein, yeast Dmc1 protein promotes strand exchange. These results open the door to future efforts to reconstitute regulated homologous recombination reactions in vitro.

We were first to show that recombination proteins can be detected at multiple subnuclear sites during recombination using immunostaining techniques. We have used this method to identify proteins trequired for recruitment of recombinase to double strand break sites in mitotic and meiotic cells. Among such regulators is the breast cancer susceptibility gene BRCA1. We have shown that BRCA1 promotes recombinase assembly and we are currently working to determine the mechanism through which BRCA1 mediates this effect

Research Papers on PubMed