Abstract
The Escherichia coli (E. coli) SOS response is the largest, most complex, and best characterized bacterial network induced by DNA damage. It is controlled by a complex network involving the RecA and LexA proteins. We have previously shown that the SOS response to DNA damage is inhibited by various elements involved in the expression of the E. coli toxin-antitoxin mazEF pathway. Since the mazEF module is present on the chromosomes of most E. coli strains, here we asked: Why is the SOS response found in so many E. coli strains? Is the mazEF module present but inactive in those strains? We examined three E. coli strains used for studies of the SOS response, strains AB1932, BW25113, and MG1655. We found that each of these strains is either missing or inhibiting one of several elements involved in the expression of the mazEF-mediated death pathway. Thus, the SOS response only takes place in E. coli cells in which one or more elements of the E. coli toxin-antitoxin module mazEF or its downstream pathway is not functioning.
Highlights
The enteric bacterium E. coli, like most other bacteria, carries on its chromosome the gene pair mazEF, belonging to the abundant family of toxin-antitoxin modules [1]. mazF specifies for the stable toxin MazF [2], a sequence specific endoribonuclease, which cleaves at ACA sites [3]. mazE specifies for the labile antitoxin MazE, which is degraded by the protease ClpPA [2]
In previous studies we showed that Extracellular Death Factor (EDF), the penta-peptide NNWNN, is involved in EDF-mazEF mediated cell death [7], and that clpX is required for the production of EDF [8]
More recently we found that the action of the mazEF module prevented the SOS response [19]; here we asked if, in addition to the mazEF module, the presence of EDF is involved in the inhibition of the SOS response
Summary
The enteric bacterium E. coli, like most other bacteria, carries on its chromosome the gene pair mazEF, belonging to the abundant family of toxin-antitoxin modules [1]. mazF specifies for the stable toxin MazF [2], a sequence specific endoribonuclease, which cleaves at ACA sites [3]. mazE specifies for the labile antitoxin MazE, which is degraded by the protease ClpPA [2]. MazF specifies for the stable toxin MazF [2], a sequence specific endoribonuclease, which cleaves at ACA sites [3]. E. coli mazEF is responsible for bacterial programmed cell death (PCD) under stressful conditions [4]. Under such conditions, the induced endoribonuclease MazF removes the 39terminal 43 nucleotides of the 16S rRNA within the ribosomes, thereby removing the anti-Shine-Dalgarno (aSD) sequence that is required for translation initiation. E. coli mazEF Pathway Inhibits the SOS Response of canonical mRNAs. Concomitantly, MazF cleaves at ACA sites at or closely upstream from the AUG start codon of certain specific mRNAs, causing the generation of leaderless mRNAs [5]. EDF induces the enoribonucleolytic activity of E. coli MazF [9]
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