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The bacterial SOS response is a cellular reaction to DNA damage, that, amongother actions, triggers the expression of colicin - toxic bacteriocins inEscherichia coli that are released to kill close relatives competing forresources. However, it is largely unknown, how the complex network regulatingtoxin expression controls the time-point of toxin release to prevent prematurerelease of inefficient protein concentrations. Here, we study how differentregulatory mechanisms affect production and release of the bacteriocinColicinE2 in Escherichia coli. Combining experimental and theoreticalapproaches, we demonstrate that the global carbon storage regulator CsrAcontrols the duration of the delay between toxin production and release andemphasize the importance of CsrA sequestering elements for the timing ofColicinE2 release. In particular, we show that ssDNA originating fromrolling-circle replication of the toxin-producing plasmid represents a yetunknown additional CsrA sequestering element, which is essential in theColicinE2-producing strain to enable toxin release by reducing the amount offree CsrA molecules in the bacterial cell. Taken together, our findings showthat CsrA times ColicinE2 release and reveal a dual function for CsrA as anssDNA and mRNA-binding protein, introducing ssDNA as an importantpost-transcriptional gene regulatory element.

CsrA and its regulators control the time-point of ColicinE2 release in Escherichia coli