作者: Cecilia Unoson , E. Gerhart H. Wagner
DOI: 10.1111/J.1365-2958.2008.06416.X
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摘要: We previously reported on an SOS-induced toxin, TisB, in Escherichia coli and its regulation by the RNA antitoxin IstR-1. Here, we addressed mode of action TisB. By placing tisB reading frame downstream a controllable promoter plasmid, toxicity could be analysed absence global SOS response. Upon induction cell growth was inhibited plating efficiency decreased rapidly. The onset correlated with drastic decrease transcription, translation replication rates. Cellular degraded, but vitro experiments showed that TisB did not affect or transcription directly. Thus, these effects are consequences membrane damage: is predicted to hydrophobic spanning, Western analyses demonstrated this peptide strictly localized cytoplasmic fraction. Membrane damage killing under multicopy expression also seen live/death staining formation ghost cells. This reminiscent another Hok plasmid R1, which targets membrane. biological significance istR/tisB locus still elusive; deletion entire gave no fitness phenotype competition experiments.