An SOS response induced by high pressure in Escherichia coli

Abstract

Although pressure is an important environmental parameter in microbial niches such as the deep sea and is furthermore used in food preservation to inactivate microorganisms, the fundamental understanding of its effects on bacteria remains fragmentary. Our group recently initiated differential fluorescence induction screening to search for pressure-induced Escherichia coli promoters and has already reported induction of the heat shock regulon. Here the screening was continued, and we report for the first time that pressure induces a bona fide SOS response in E. coli, characterized by the RecA and LexA-dependent expression of uvrA, recA, and sulA. Moreover, it was shown that pressure is capable of triggering lambda prophage induction in E. coli lysogens. The remnant lambdoid e14 element, however, could not be induced by pressure, as opposed to UV irradiation, indicating subtle differences between the pressure-induced and the classical SOS response. Furthermore, the pressure-induced SOS response seems not to be initiated by DNA damage, since DeltarecA and lexA1 (Ind-) mutants, which are intrinsically hypersensitive to DNA damage, were not sensitized or were only very slightly sensitized for pressure-mediated killing and since pressure treatment was not found to be mutagenic. In light of these findings, the current knowledge of pressure-mediated effects on bacteria is discussed.

FIG. 1.

Flow-cytometry analysis of the high-pressure induction of PuvrA, PrecA, and PsulA fused to gfp in the wild-type MG1655 background, 3 h after treatment at 100 MPa for 15 min. The curves with the grey and transparent surfaces underneath represent populations of approximately 10⁵ control cells and high-pressure-treated cells, respectively.

FIG. 2.

High-pressure (100 MPa, 15 min, ▪) and UV (0.1 kJ/m², ▴) induction of PuvrA, PrecA, and PsulA fused to gfp in the wild-type MG1655, ΔrecA, and lexA1 (Ind⁻) backgrounds compared to results for untreated control cells (♦).

FIG. 3.

(A) Induction of phage λ lysogens by high-pressure treatment (100 MPa, 15 min). Evolution of phage particle count [log(PFU/ml)] in untreated (▴) and high-pressure-treated (▪) cell suspensions of MG1655. (B) Fold increase in phage particle count (PFU/ml) 3 h after pressure treatment (100 MPa, grey bars) or UV treatment (0.1 kJ/m², dashed bars) in cell suspensions of the MG1655 wild type or ΔrecA or lexA1 mutant. Titers of phage for untreated cell suspensions were ca. 1.2 × 10³ PFU/ml for wild-type lysogens, 5 PFU/ml for ΔrecA lysogens, and 3.5 × 10³ PFU/ml for lexA1 lysogens.

FIG. 4.

Number of survivors [log(N)] of wild-type (▪), ΔrecA (♦), and lexA1 (▴) cells of MG1655 after treatment at different pressures (A) or with different doses of UV (B). No survivors were recovered upon UV treatment of the ΔrecA and lexA1 cells at doses of ≥20 J/m².