Auto-regulation of DNA degrading bacteriocins: molecular and ecological aspects

Abstract

Colicins, proteinaceous antibiotics produced by Escherichia coli, specifically target competing strains killing them through one of a variety of mechanisms, including pore formation and nucleic acid degradation. The genes encoding colicins display a unique form of expression, which is tightly regulated, involving the DNA damage response regulatory system (the SOS response system), confined to stressful conditions and released by degradation of the producing cell. Given their lethal nature, colicin production has evolved a sophisticated system for repression and expression. While exploring the expression of 13 colicins we identified a novel means of induction unique to strains that kill by DNA degradation: these colicinogenic strains mildly poison themselves inflicting DNA damage that induces their DNA repair system (the SOS system), and their own expression. We established that among the four known DNase colicins (E2, E7, E8 and E9), three act to induce their own production. Using different stresses we show that this form of self-regulation entails high cost when growth conditions are not optimal, and is not carried out by individual cells but is a population-mediated trait. We discuss this novel form of colicins' regulation and expression, and its possible molecular mechanism and evolutionary implications.

Effects of stochasticity and division of labor in toxin production on two-strain bacterial competition in Escherichia coli

“…coli . Here, similar to many other colicins [25], phenotypic heterogeneity is a consequence of the regulation via the noisy SOS response [26,28,29], which can be triggered by the inducing agent mitomycin C (MitC) [25], with higher MitC levels increasing the fraction of toxin producers [30]. The dynamics of ColicinE2 production have been investigated in detail [30].…”

Amount of Colicin Release in Escherichia coli Is Regulated by Lysis Gene Expression of the Colicin E2 Operon

“…coli bacteria or other members of the Enterobacteriaceae [ 5 ]. Experimental studies focus on the mechanism of colicin release [ 9 – 11 ], colicin uptake by strains sensitive to the bacteriocin [ 12 , 13 ], or the evolutional and ecological importance of colicins [ 4 , 5 , 14 , 15 ]. In contrast, the majority of the theoretical investigations have been studying the interplay of colicin-producing bacteria with bacteria that are sensitive to or resistant against the bacteriocin [ 16 – 21 ].…”

The Evolution of Mass Cell Suicide in Bacterial Warfare

“…Producing cells permeabilize their own membrane with a dedicated lysis protein to release toxins into the environment, killing themselves in the process [1–3]. When a colicin producing strain is growing alone, the colicin operon is typically only expressed in a small fraction of the population [9–15]. Expression can be upregulated by DNA damage as the colicin operon is regulated by the SOS response pathway [14,16,17], which is often done artificially via the addition of DNA-damaging agents such as mitomycin C [12,14,16,18,19].…”

“…Bacteria often grow in dense biofilms or host-associated communities, where cell-cell interactions between clonemates - in addition to interactions between genotypes - can play a key role in their behaviours [30,33–35]. In the case of colicins, the production of some DNase colicins - including colicin E2 - can be induced by the presence of the same colicins released by clonemates, a phenomenon termed autoinduction [9,15,36]. We therefore sought to follow the lysis response in bacterial colonies at high cell density, where autoinduction is expected to be maximal.…”