In surface adapted bacteria, such as Escherichia coli, high pressure (HP) shock greatly perturbs cellular homeostasis. Nevertheless, the cellular impact of HP stress and the actual damage it provokes remain poorly characterized. Using the Differential Fluorescence Induction (DFI) technique coupled to fluorescence activated cell sorting, we have studied the response of E. coli to sublethal HP shock (< 150 MPa). It was found that HP shock induces several genes belonging to the heat shock regulon, and also genes belonging to the SOS regulon. Since the SOS response is a response to DNA damage, and HP is not known to cause direct DNA damage, the mechanism of SOS induction was further analysed in more detail. It was shown that SOS induction stems from the HP mediated activation of the restriction endonuclease Mrr and the subsequent formation of double stranded DNA breaks, which trigger a genuine RecA and LexA dependent  SOS response. Several phenotypes linked to SOS induction were observed, including the induction of prophage and cell filamentation. The SOS response is also anticipated to cause an increased mutation rate, and this is indeed supported by some experimental observations.

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