The bacterial SOS response is not only a vital reply to DNA damage but also constitutes an essential mechanism for the generation of genetic variability that in turn fuels adaptation and resistance development in bacterial populations. Despite the extensive depiction of the SOS regulon itself, its activation by stresses different from typical DNA damaging treatments remains poorly characterized. Recently, we reported the RecA- and LexA-dependent induction of the SOS response in Escherichia coli MG1655 after exposure to high hydrostatic pressure (HP, similar to 100 MPa), a physical stress of which the cellular effects are not well known. We now found this HP mediated SOS response to depend on RecB and not on RecF, which is a strong indication for the involvement of double strand breaks. As the pressures used in this work are thermodynamically unable to break covalent bonds in DNA, we hypothesized the involvement of a cellular function or pathway in the formation of this lesion. A specialized screening allowed us to identify the cryptic type IV restriction endonuclease Mrr as the final effector of this pathway. The HP SOS response and its corresponding phenotypes could be entirely attributed to the HP triggered activation of Mrr restriction activity. Several spontaneously occurring alleles of mrr, incapable of triggering the HP-induced SOS response, were isolated and characterized. These results provide evidence for a specific pathway that transmits the perception of HP stress to induction of the SOS response and support a role for Mrr in bacterial stress physiology.