Abstract
The production of bacteriocins in response to worsening environmental conditions is one means of bacteria to outcompete other microorganisms. Colicins, one class of bacteriocins in Escherichia coli, are effective against closely related Enterobacteriaceae. Current research focuses on production, release and uptake of these toxins by bacteria. However, little is known about the quantitative aspects of these dynamic processes. Here, we quantitatively study expression dynamics of the Colicin E2 operon in E. coli on a single cell level using fluorescence time-lapse microscopy. DNA damage, triggering SOS response leads to the heterogeneous expression of this operon including the cea gene encoding the toxin, Colicin E2, and the cel gene coding for the induction of cell lysis and subsequent colicin release. Advancing previous whole population investigations, our time-lapse experiments reveal that at low exogenous stress levels all cells eventually respond after a given time (heterogeneous timing). This heterogeneous timing is lost at high stress levels, at which a synchronized stress response of all cells 60 min after induction via stress can be observed. We further demonstrate, that the amount of colicin released is dependent on cel (lysis) gene expression, independent of the applied exogenous stress level. A heterogeneous response in combination with heterogeneous timing can be biologically significant. It might enable a bacterial population to endure low stress levels, while at high stress levels an immediate and synchronized population wide response can give single surviving cells of the own species the chance to take over the bacterial community after the stress has ceased.
Highlights
Bacteria possess several mechanisms enabling them to respond to changing and unfavorable environmental conditions or to outcompete other bacteria [1,2,3,4,5]
We present the first quantitative analysis of the expression dynamics of the Colicin E2 operon in E. coli
Using single cell time-lapse microscopy, we thereby distinguished between the expression dynamics of the cea gene encoding the toxin Colicin E2 and the cel gene responsible for colicin release
Summary
Bacteria possess several mechanisms enabling them to respond to changing and unfavorable environmental conditions or to outcompete other bacteria [1,2,3,4,5]. 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 [16,17,18,19,20,21]. Toxins, such as the bacteriocin Colicin E2 of this study, are plasmid encoded and expressed from operons under the control of an SOS promoter [8, 22, 23].
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