Sequence of the relB transcription unit from Escherichia coli and identification of the relB gene.

Abstract

Escherichia coli relB mutants react to amino acid starvation by several abnormal responses, including accumulation of a translational inhibitor. We have isolated a relB‐complementing plasmid from the Clarke and Carbon E. coli DNA library. From this plasmid we sequenced a 2140‐bp segment which included the relB gene by the following two criteria: (i) it complements chromosomal relB mutations, (ii) the corresponding DNA segment cloned from chromosomal DNA of three relB mutants was defective in relB complementation. All three mutations fell within an open reading frame of 79 amino acids. A polypeptide of 9 kd compatible with this open reading frame was synthesized in maxicells and is in all probability the product of the relB gene. By nuclease S1 mapping we have determined the transcription start and stop of an 870 base transcript of the relB gene.

Molecular Control of Bacterial Death and Lysis

“…However, the "delayed-relaxed" phenotype observed in RelB mutants is characterized by the production of stable RNAs that resumes after a 10-min lag period following amino acid starvation (52,53). The locus responsible for the delayed-relaxed phenotype was sequenced and identified by Bech et al (17) and was found to contain a three-gene operon comprised of the relB, relE, and relF genes. The relF open reading frame displayed both functional and structural similarity to the hok gene of plasmid R1, whose gene product is responsible for the postsegregational killing of cells that lose plasmid R1 during cell division (79,81).…”

A Novel Family of Escherichia coli Toxin-Antitoxin Gene Pairs

“…Alternatively, examination of the toxinantitoxin gene pair relB/relE (12,17,19,31,32) supports the model that, unlike plasmid-based toxins, the function of the chromosomal TA pairs is not bacterial "apoptosis" but to modulate the rate of metabolic processes in response to environmental stress (18). Mutant alleles of relB confer a defect in the stringent response termed a delayed relaxed phenotype, in which cells are unable to efficiently resume protein synthesis after readdition of amino acids (4,15,24). Excess RelE protein has been shown to result in a decrease in the rate of protein synthesis both in vitro and in vivo, and this inhibition is neutralized by the addition of the antitoxin RelB (12,31).…”

mazEF: a chromosomal toxin-antitoxin module that triggers programmed cell death in bacteria

“…coli, there are several toxin-antitoxin systems, including mazEF (Metzger et al, 1988;Masuda et al, 1993;Aizenman et al, 1996;Engelberg-Kulka et al, 2004), chpBIK (Masuda et al, 1993;Masuda and Ohtsubo, 1994), relBE (Bech et al, 1985;Gotfredsen and Gerdes, 1998;Gerdes et al, 2005), yefMyoeB (Grady and Hayes, 2003;Cherney and Gazit, 2004;Christensen et al, 2004) and dinJ-yafQ (Hayes, 2003). The most studied among these is mazEF, which was the first to be discovered and described as regulatable and responsible for bacterial PCD (Metzger et al, 1988;Masuda et al, 1993;Aizenman et al, 1996).…”