RecA is a bacterial protein that functions in at least two ways to repair DNA damage. First, it has a DNA strand exchange activity that catalyzes recombinational DNA repair. Second, it has a coprotease activity that regulates the expression of SOS genes which also are involved in DNA repair. The primary goal of this work is to determine the molecular basis underlying RecA-dependent DNA repair. The proposed research involves the use of genetic, molecular biological, biochemical and protein design techniques aimed at defining both RecA-specific repair events, as well as functional interactions between RecA protein and other SOS gene products that contribute to the overall process of DNA repair. This investigator has devised a genetic system in which expression of the RecA gene is controlled by Ptac, thereby removing RecA from the autoregulatory SOS pathway. This system has allowed the identification of mutants with distinct split phenotypes which will facilitate in the dissection of this repair pathway.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
1R29CA068290-01
Application #
2112209
Study Section
Chemical Pathology Study Section (CPA)
Project Start
1995-07-01
Project End
2000-06-30
Budget Start
1995-07-01
Budget End
1996-06-30
Support Year
1
Fiscal Year
1995
Total Cost
Indirect Cost
Name
University of Massachusetts Medical School Worcester
Department
Biochemistry
Type
Schools of Medicine
DUNS #
660735098
City
Worcester
State
MA
Country
United States
Zip Code
01655