In addition to being an essential component of trans‐lesion synthesis, the UmuD′C complex is an antagonist of RecA‐mediated homologous recombination. When constitutively expressed at an elevated concentration, the UmuD′C complex sensitizes recA+ bacteria to DNA damage, whereas it has no effect on bacteria expressing a RecA [UmuR] protein that overcomes recombination inhibition. Using as a genetic screen enhanced cell killing on mitomycin plates, we isolated novel umuD′ and umuC mutations that restored mitomycin sensitivity to recA D112G [UmuR] bacteria overproducing the UmuD′C complex. The mutations were named [Rin++] because a characterization in a recA+ as well in a recA D112G background showed that they enhanced UmuD′C‐promoted recombination inhibition in two assays, conjugational recombination and recombinational repair of palindrome‐containing DNA. The [Rin++] mutations affect five amino acids, G25D, S28T, P29L, E35K, and T95R, in UmuD′ and seven, F10L, Y270C, K277E, F287L, F287S, K342Q and F351I, in UmuC. These amino acids might play a key role in the UmuD′C anti‐recombination activity. None of the [Rin++] mutations enhanced UmuD′C‐promoted mutagenic bypass of UV lesions, in contrast, several lead to a defect in this process. In this study, we discuss a few molecular mechanisms that could account for the recombination and mutagenesis phenotypes of a mutant UmuD′C [Rin++] complex.