Figure 2.

Illustration of the two classes of extended translesion synthesis products observed by Reuven et al. (8). In the absence of UmuD′₂ and UmuC, the translesion synthesis product most commonly carried a 1-nt deletion that apparently arose by a slippage mechanism. In the presence of UmuD′₂ and UmuC, the predominant translesion synthesis product was of the expected length and apparently rose from the introduction of a nucleotide, most often an A, opposite the abasic site.