Abstract
The SOS response addresses DNA lesions and is conserved in the bacterial domain. The response is governed by the DNA binding protein LexA, which has been characterized in model microorganisms such as Escherichia coli. However, our understanding of its roles in deep-sea bacteria is limited. Here, the influence of LexA on the phenotype and gene transcription of Shewanella piezotolerans WP3 (WP3) was investigated by constructing a lexA deletion strain (WP3ΔlexA), which was compared with the wild-type strain. No growth defect was observed for WP3ΔlexA. A total of 481 and 108 genes were differentially expressed at 20 and 4°C, respectively, as demonstrated by comparative whole genome microarray analysis. Furthermore, the swarming motility and dimethylsulfoxide reduction assay demonstrated that the function of LexA was related to temperature. The transcription of the lexA gene was up-regulated during cold acclimatization and after cold shock, indicating that the higher expression level of LexA at low temperatures may be responsible for its temperature-dependent functions. The deep-sea microorganism S. piezotolerans WP3 is the only bacterial species whose SOS regulator has been demonstrated to be significantly influenced by environmental temperatures to date. Our data support the hypothesis that SOS is a formidable strategy used by bacteria against various environmental stresses.
Highlights
Since it was first described by Radman (1975), the detailed pathway of the SOS response to DNA lesions had been thoroughly investigated in the model bacterium Escherichia coli
No significant filament phenotype was observed, the cell length of the lexA mutant was notably increased at 2.33 (4◦C) – 4.43 (20◦C), indicating that the lexA deletion had an effect on cell division and morphology (Supplementary Figure S2)
Previous studies showed that the lexA gene deletion was lethal for E. coli and other γ-proteobacteria, such as Pseudomonas putida, P. aeruginosa, Aeromonas hydrophila, Erwinia carotovora, and Salmonella typhimurium (Walker, 1984; Calero et al, 1993; Riera and Barbe, 1995)
Summary
Since it was first described by Radman (1975), the detailed pathway of the SOS response to DNA lesions had been thoroughly investigated in the model bacterium Escherichia coli. Stress-survival studies showed that an SOS-deficient mutant of Listeria monocytogenes was less resistant to heat (55◦C), H2O2 and acid exposure (pH 3.4) compared to the wild-type cells (van der Veen et al, 2010). Studies have demonstrated the crucial role of the SOS response in promoting the spread of mobile genetic elements (Beaber et al, 2003) and integron recombination, which are responsible for incorporating and expressing genes grouped as cassettes (Guerin et al, 2009). SOS plays a considerable role in lateral gene transfer and evolution
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