coli FC40 system under carbon

starvation conditions and for the emergence of tetracycline-resistant mutants in response to antibiotic (tetracycline) treatment. NusA, a modulator of RNA polymerase, was previously shown to interact with Pol IV (Cohen et al., 2009). Hence, a model is proposed that DNA replication initiated during DSBR could generate DNA substrates that will stall RNA polymerase and lead to the recruitment of Pol IV by NusA (Cohen & Walker, 2010). The LexA regulon of P. aeruginosa and P. putida is significantly smaller than that of E. coli (Courcelle et al., 2001; Cirz et al., Vismodegib nmr 2005; Abella et al., 2007). Among the specialized DNA polymerases, the transcription of the Pol II gene polB is not induced by DNA damage in these organisms. Although the Pol IV gene dinB promoter has a LexA-binding site and the level of transcription

from this promoter is slightly increased in Pseudomonas species in the presence of DNA-damaging agents (Tegova et al., 2004; Cirz et al., 2005; Abella et al., 2007), the extent of SOS induction is considerably smaller than that observed in E. coli. Compared with E. coli, pseudomonads seem to have evolved a regulatory system allowing a significantly high basal level of particular SOS regulon genes already in the absence of this website DNA damage. Notably, the promoters of P. putida dinB gene and rulAB genes (encoding the Pol V homologue on toluene catabolic plasmid), both of which contain the LexA-binding site, are highly inducible by DNA damage LY294002 in E. coli, whereas in P. putida, they express already at a considerably high basal level (Tegova et al., 2004; Tark et al., 2005). This indicates that the P. putida LexA repressor has evolved a lower affinity to its target sites compared with E. coli LexA. Importantly, the majority of bacteria, including pseudomonads, lack chromosomal Pol V genes umuD and umuC, but instead carry a

multiple gene cassette encoding a second copy of the α-subunit of DNA polymerase III and a protein related to Y-family DNA polymerases, DnaE2 and ImuB, respectively (Abella et al., 2004; Erill et al., 2006; Koorits et al., 2007). Similar to the Pol V genes, these genes are induced by DNA damage. In P. putida this gene cluster is negatively controlled by another LexA repressor, LexA2, which binds the DNA sequence GTACN4GTGC (Abella et al., 2004, 2007). The binding site of LexA2 differs completely from that recognized by E. coli-like LexA, which binds the classical CTGTN8ACAG box. Pseudomonas aeruginosa has only one LexA protein, which is related to E. coli LexA, and the imuB and dnaE2-containing gene cluster of P. aeruginosa is negatively controlled by this LexA (Cirz et al., 2005). The gene cluster similar to that identified in P. putida (Abella et al., 2004) or part of it has been identified in many families of Proteobacteria (Abella et al., 2004; Erill et al., 2006).