ImuB and ImuC contribute to UV‐induced mutagenesis as part of the SOS regulon in Pseudomonas aeruginosa

Abstract

DNA damage‐induced mutagenesis is a process governed by the SOS system that requires the activity of specialized DNA polymerases. These polymerases, which are devoid of proof‐reading activity, serve to increase the probability of survival under stressful conditions in exchange for an error‐prone DNA synthesis. As an opportunistic pathogen of humans, Pseudomonas aeruginosa employs adaptive responses that originally evolved for survival in many diverse and often stressful environmental conditions, where the action of error‐prone DNA polymerases may be crucial. In this study, we have investigated the role of the polymerases ImuB and ImuC in P. aeruginosa DNA‐damage induced mutagenesis. UV irradiation of imuB‐ and imuC‐deletion mutants showed that both genes contribute to UV‐induced mutagenesis in this bacterium. Furthermore, we confirmed that UV treatment significantly increase the expression levels of the imuB and imuC genes and that they are co‐transcribed as a single transcriptional unit under the control of LexA as part of the SOS regulon in P. aeruginosa. Environ. Mol. Mutagen. 2019. © 2019 Wiley Periodicals, Inc.

RecA and Specialized Error-Prone DNA Polymerases Are Not Required for Mutagenesis and Antibiotic Resistance Induced by Fluoroquinolones in Pseudomonas aeruginosa

“…Notably, we observed a comparable induction of resistance frequency by ciprofloxacin in all mutants, irrespective of the presence or absence of RecA (Figure 2b). Thus, even if DinB and ImuBC were previously reported to play a role in the tolerance of P. aeruginosa to DNA damages, such as those induced by alkylating agents and ROS [52][53][54], and ImuBC was also found to contribute to UV-induced mutagenesis [40], our results strongly suggest that none of the specialized DNA polymerases of P. aeruginosa is required for the fluoroquinolone-mediated increase in the mutation rate. also in the ΔrecA mutant, implying that the antibiotic triggers the expression of these genes through an SOS-independent mechanism.…”

“…To validate the role of RecA in the activation of the SOS response in P. aeruginosa, the expression of four genes, which were previously demonstrated to belong to the P. aeruginosa SOS regulon by independent studies [23,25,31,39,40], was evaluated in PAO1 and ∆recA by quantitative reverse transcription PCR (qRT-PCR). In order to set up the right conditions to induce the SOS stress response under sub-lethal doses of antibiotic, the susceptibility of the wild type and ∆recA strains to ciprofloxacin was preliminarily assessed by MIC assays.…”

Coexistence of SOS-Dependent and SOS-Independent Regulation of DNA Repair Genes in Radiation-Resistant Deinococcus Bacteria

“…SOS mutagenesis by this cassette has been studied in particular in Caulobacter crescentus (Caulobacter vibrioides) [41,43], Mycobacterium tuberculosis [44,45] and Pseudomonas spp. [46][47][48]. ImuA and ImuB are accessory factors required for the error-prone TLS performed by DnaE2 (also called ImuC), a paralog of the α subunit DnaE of the bacterial replicative polymerase.…”

Prophage Activation in the Intestine: Insights Into Functions and Possible Applications

“…By using single-molecule imaging techniques for live cells, it was proved that the RecA protein was sequestered in storage structures until DNA damage happened, and early SOS-signaling complexes were formed subsequently ( Ghodke et al, 2019 ). The polymerases ImuB and ImuC acting as factors involved in the regulation of SOS system were co-transcribed under the control of LexA in Pseudomonas aeruginosa ( Luján et al, 2019 ). The exo-xis region of lambdoid bacteriophages and OxyR regulator influenced prophage maintenance and induction ( Bloch et al, 2013 ; Licznerska et al, 2015 ).…”