Bhavik Kumar is a graduate of Corsicana High School, class of 2002. He is currently in his third year here at Southwestern University as a full-time undergraduate student. He plans to pursue Bachelor of Science degrees in both Biology and Chemistry. Upon graduation, he would like to continue his education in the medical  sciences.  To learn more about me, click here.

RESEARCH PROJECT 

The E. coli SOS response to DNA damage is controlled by two proteins, LexA and RecA. Following exposure to DNA damaging agents, the replicative polymerase DNA pol III stalls at DNA lesions creating regions of single stranded DNA. This stimulates the RecA protein to undergo a change from its normal physiological state to an activated one referred to as RecA*.  Preliminary studies suggest that RecA* is similarly stimulated by induction of inorganic polyphosphate (polyP) synthesis. PolyP has been shown to be involved in processes ranging from gene expression to protein degradation. This project focuses on the role of polyP in stimulating the activation of RecA to RecA*. It stems from the broader research interests of Gonzalez on the regulation of SOS mutagenesis and Rawji on the investigation of phosphate esters using NMR spectroscopy.

            We postulate that polyP mimics the negatively charged phosphate backbone of single-stranded DNA in attracting RecA. In this study, the genes required for polyP production will be deleted so that polyP levels can be controlled. Some questions we hope to answer in this investigation are: How and where on RecA does polyP bind? Does polyP chain length differentially affect activation? Once bound, what sequence of events leads to activation of RecA?

We propose a dual track, complementary investigation of how polyP activates RecA. The in vivo studies will investigate DNA polymerase V activity in polyP deficient strains.  Moreover, NMR spectroscopy (¹H and ³¹P) will be used to probe the RecA structure in its unbound state in order to follow the conformational changes resulting from binding with polyP.