Abstract
Colicins are plasmid-encoded narrow spectrum antibiotics that are synthesized by strains of Escherichia coli and govern intraspecies competition. In a previous report, we demonstrated that the global transcriptional factor IscR, co dependently with the master regulator of the DNA damage response, LexA, delays induction of the pore forming colicin genes after SOS induction. Here we show that IscR is not involved in the regulation of nuclease colicins, but that the AsnC protein is. We report that AsnC, in concert with LexA, is the key controller of the temporal induction of the DNA degrading colicin E8 gene (cea8), after DNA damage. We demonstrate that a large AsnC nucleosome-like structure, in conjunction with two LexA molecules, prevent cea8 transcription initiation and that AsnC binding activity is directly modulated by L asparagine. We show that L-asparagine is an environmental factor that has a marked impact on cea8 promoter regulation. Our results show that AsnC also modulates the expression of several other DNase and RNase colicin genes but does not substantially affect pore-forming colicin K gene expression. We propose that selection pressure has “chosen” highly conserved regulators to control colicin expression in E. coli strains, enabling similar colicin gene silencing among bacteria upon exchange of colicinogenic plasmids.
Highlights
Colicins are high-molecular-weight toxic proteins that are produced by and target Escherichia coli and its close relatives [1]
IscR does not regulate the induction of the DNA or RNA degrading colicins To study the induction of various nuclease colicins after DNA damage, we assayed the activity of colicin promoters in E. coli K-12 strain BW25113
To determine if a similar mechanism controls the expression of the nuclease colicins, we investigated the regulation of the DNA degrading colicin E8 by electrophoretic mobility-shift assays (EMSA) and DNase I footprinting
Summary
Colicins are high-molecular-weight toxic proteins that are produced by and target Escherichia coli and its close relatives [1]. These narrow-spectrum antibiotics kill by either targeting the DNA, RNA or cell membranes of susceptible cells. Cytoplasmic colicins are released upon the synthesis of a lysis protein, the expression of which is independent of intracellular colicin accumulation [2]. This causes the stochastic lysis of producing cells and is suggested to assist surviving sister cells by killing potential competing sensitive cells [3]. Nutrient limitation and DNA damage seem to be the major signals that control colicin production, enabling interference competition among strains [8]
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