Efforts to study the role of gut microbiota on human health are hampered by the ability to manipulate specific species and strains. For this reason, CRISPR-Cas9 has become a valuable molecular tool due to its ability to be programmed to target a specific sequence. The conjugative transfer of a plasmid encoding Cas9 from E. coli to S. enterica has already been demonstrated, thus presenting an avenue for in-situ microbiota manipulation. In E. coli, a double strand break introduced by Cas9 is lethal if not repaired by the recBCD recombination pathway. An alternative recombination pathway in E. coli is via recF. Recently, a DNA ADP-ribosyltransferase (DarT) enzyme that functions as a bacterial defense toxin, has been shown to install a replication blocking lesion, that in the absence of its cognate antitoxin (DarG), leads to polymerase skipping, and the formation of a ssDNA gap. This ssDNA gap is then repaired by the recF recombination pathway. Here we demonstrate a novel gene editing system, by which a fusion of DarT to an inactivated Cas9 drives recombination in E. coli without the generation of a double strand break. Using a gene conversion assay in which a span of 8 bases are substituted, we show that our system of editing is comparable in efficiency to standalone Cas9-driven recombination, but an order of magnitude less toxic. Next, we demonstrate the ability to substitute upwards of 60 bases in either direction of the target site, in addition to insertions of 100 bases centered on the target site, and deletions of 60 bases surrounding the target site. We confirm that gene editing is dependent on the recF recombination pathway. Finally we demonstrate conjugative transfer of the system, and successive gene conversion in an E. coli host/recipient co-culture, at an efficiency that exceeds standalone Cas9 by an order of magnitude, while also an order of magnitude less toxic. DarT is the first of what we believe will become a new category of gene editors centered upon harnessing enzymes which modify DNA, in order to drive endogenous DNA repair pathways for purposes of gene editing, without generating double strand breaks.