Whereas the absence of DnaE2 increases the frequency of mutations, the lack of ImuB has a negative effect on the mutation frequency (Koorits et al., 2007). There is a competition of different DNA polymerases for binding to the β-clamp to take over the DNA synthesis (Johnson & O’Donnell, 2005).

For example, in E. coli Pol II competes with Pol IV SCH727965 datasheet on stationary-phase mutagenesis and limits Pol IV’s mutagenic activity (Layton & Foster, 2003). Thus, one may speculate that ImuB (like eukaryotic Rev1) serves as a scaffold protein for the recruitment of various DNA polymerases. As already mentioned above, bacteria that carry the dnaE2-containing operon lack umuDC genes in their chromosome. This raises an interesting question of whether the coexistence of these two operons in the same bacterium would be disadvantageous under certain circumstances. Several studies indicate that this is not the case. For example, the Pol V homologue RulAB encoded by toluene catabolic plasmid (TOL plasmid) pWW0

increases the survival of P. putida under conditions of DNA damage (Tark et al., 2005). Moreover, P. putida carrying the rulAB STA-9090 genes introduced into the chromosome expresses a strong GASP phenotype. Thus, this DNA polymerase significantly increases the evolutionary fitness of bacteria during prolonged nutritional starvation of a P. putida population, which indicates that RulAB increases the probability of accumulation of

beneficial mutations, allowing genetic adaptation of bacterial populations under conditions of environmental stress. Another study by Saumaa et al. (2007) revealed that although the frequency of accumulation of stationary-phase mutations in P. putida was not significantly affected by the presence of the rulAB genes, some differences appeared in the spectra of base substitutions. Namely, the introduction of rulAB into P. putida increased the proportion of Cepharanthine A-to-C and A-to-G base substitutions among mutations, which occurred under starvation conditions, implying that RulAB may perform mutagenic TLS past damaged adenine. umuDC orthologues are widely distributed in broad-host-range catabolic and antibiotic resistance plasmids (Permina et al., 2002; Tark et al., 2005). Such plasmids have contributed significantly to virulence and ecological fitness in bacteria. For example, Pseudomonas strains harboring umuDC orthologues rulAB on plasmids have increased UV tolerance, enabling bacteria to survive on leaf surfaces that are exposed to DNA-damaging UV irradiation (Sundin & Murillo, 1999). Hence, the question arises: why do these genes locate usually on plasmids and not in the bacterial chromosome? Under the conditions of environmental stress that leads to the accumulation of DNA damage in a cell, the activation of DNA polymerase Pol V increases the survival of cells due to continuing DNA synthesis by Pol V at damaged sites.