Abstract
Toxin-antitoxin (TA) modules are gene pairs specifying for a toxin and its antitoxin and are found on the chromosomes of many bacteria including pathogens. Here we report how each of five such TA systems in E. coli affect bacterial cell death differently in liquid media and during biofilm formation. Of all these systems, only the TA system mazEF mediated cell death both in liquid media and during biofilm formation. At the other extreme, as our results have revealed here, the TA system dinJ-YafQ is unique in that it is involved only in the death process during biofilm formation. Cell death governed by mazEF and dinJ-YafQ seems to participate in biofilm formation through a novel mechanism.
Highlights
Toxin-antitoxin systems consist of a pair of genes that specify two components: a stable toxin and an unstable antitoxin that interferes with the action of the toxin
Here, using similar experimental conditions, we compared the effects on cell death of the five confirmed E. coli TA systems in liquid media and in bioifilm formation. We found that these TA systems can be divided into four groups: 1) mazEF is involved in the death processes in both liquid and biofilm formation; 2) relBE only participates in cell death in liquid medium; 3) chpBIK and yefM-yoeB only participate in cell death in liquid medium under certain conditions; and 4) dinJ-yafQ only participates in the death process involved in biofilm formation, but not in liquid medium
We found that overproducing each of these E. coli toxins led to significantly different results (Figure 1A): The most rapid and dramatic loss of viability was caused by overproducing either MazF or RelE: in only one hour, the number of colony forming units was decreased by 3 orders of magnitude, in 6 hours by more than 4 orders of magnitude
Summary
Toxin-antitoxin systems consist of a pair of genes that specify two components: a stable toxin and an unstable antitoxin that interferes with the action of the toxin. Any stressful condition that prevents the expression of the chromosomally borne mazEF module will lead to the reduction of MazE in the cell, permitting toxin MazF to act freely. Such conditions include: (i) antibiotics inhibiting transcription and/or translation like rifampicin, chloramphenicol, and spectinomycin [15]; and ii) antibiotics causing DNA damage like trimethiprim or nalidixic acid [16,17]. These antibiotics, and some other stressful conditions that are well known to cause bacterial cell death [18,19], have been found to act through the mazEF module [15,16,17]
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