Suppression of template switching in postreplication gaps via Uup and RadD proteins

Abstract

We are investigating the role of two bacterial proteins, RadD and Uup, in suppressing genomic stability. Uup is a UvrA‐like ABC family ATPase and RadD is a RecQ‐like SF2 family ATPase. Both of these proteins bind to branched DNAs. More specifically, RadD suppresses crossover events in the cell. The proteins resolve branched DNA intermediates that have arisen from template switching in post replication gaps. When a replication fork comes upon a lesion in the DNA, and a gap forms, the cell attempts to fill this gap and repair the DNA. One way of doing this is through template switching, a RecA‐independent process that creates recombination‐like branched DNA intermediates. These are the DNA intermediates at which RadD and Uup function. When genomic repeats exist in the chromosome, template switching sometimes results in mispairing that produces genomic deletions. Under normal growth conditions, with repeats in the chromosome, the deletion of Uup and RadD leads to the generation of chromosomal dimers that are not readily resolved. This experiment brings light to the functions of both proteins and recognizes the importance of genomic stability for cell viability. The results indicate that template switching happens often and that Uup and RadD play important roles in suppressing genomic stability.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.