Mrr instigates the SOS response after high pressure stress in Escherichia coli

摘要: 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 populations. Despite extensive depiction regulon itself, its activation by stresses different from typical damaging treatments remains poorly characterized. Recently, we reported RecA- LexA-dependent induction Escherichia coli MG1655 after exposure high hydrostatic pressure (HP, approximately 100 MPa), physical stress which cellular effects are well known. We now found this HP mediated depend on RecB RecF, strong indication involvement double strand breaks. As pressures used work thermodynamically unable break covalent bonds DNA, hypothesized function or pathway formation lesion. A specialized screening allowed us identify cryptic type IV restriction endonuclease Mrr as final effector pathway. corresponding phenotypes could be entirely attributed triggered activity. Several spontaneously occurring alleles mrr, incapable triggering HP-induced response, were isolated These results provide evidence specific transmits perception support role physiology.