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PubMed1963

[ALLERGIC SHOCK].

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Adrenocorticotropic Hormone↗
PubMed2004

Interference of mRNA function by sequence-specific endoribonuclease PemK.

In Escherichia coli, programmed cell death is mediated through the system called "addiction module," which consists of a pair of genes encoding a stable toxin and a labile antitoxin. The pemI-pemK system is an addiction module present on plasmid R100. It helps to maintain the plasmid by post-segregational killing in E. coli population. Here we demonstrate that purified PemK, the toxin encoded by the pemI-pemK addiction module, inhibits protein synthesis in an E. coli cell-free system, whereas the addition of PemI, the antitoxin against PemK, resumes the protein synthesis. Further studies reveal that PemK is a sequence-specific endoribonuclease that cleaves mRNAs to inhibit protein synthesis, whereas PemI blocks the endoribonuclease activity of PemK. PemK cleaves only single-stranded RNA preferentially at the 5' or 3' side of the A residue in the "UAH" sequences (where H is C, A, or U). Upon induction, PemK cleaves cellular mRNAs to effectively block protein synthesis in E. coli. The pemK homologue genes have been identified on the genomes of a wide range of bacteria. We propose that PemK and its homologues form a novel endoribonuclease family that interferes with mRNA function by cleaving cellular mRNAs in a sequence-specific manner.

Base Sequence↗
PubMed1969

Activity of diphtheria toxin. II. Early events in the intoxication of HeLa cells.

The initial steps in the interaction of diphtheria toxin with HeLa cells were studied. It was demonstrated that lethal doses of toxin are rapidly adsorbed to the cell. The kinetics of uptake, as measured by lethality, indicated that a single toxin molecule is able to cause cell death. Studies on the effect of pH on intoxication showed that adsorption of toxin occurred over a wide pH range but was partially inhibited at high pH values. Experiments to determine the influence of the ionic environment on intoxication indicated that adsorption of toxin did not take place in the absence of salts and was partially inhibited in the presence of a polyanion. The evidence indicates that the initial binding of toxin to the cell is electrostatic in nature, involving positively charged surface groups. Attempts to demonstrate specific receptors for the attachment of toxin to cells were unsuccessful, suggesting that toxin adsorption may be a nonspecific process. The effect of energy inhibitors on intoxication was examined. Sodium fluoride, an inhibitor of glycolysis, almost completely prevented intoxication in HeLa cells, whereas inhibitors of respiration and oxidative phosphorylation had no effect. Sodium fluoride did not prevent adsorption of toxin but appeared to inhibit a later step in the intoxication process, perhaps the transport of toxin to subsurface or intracellular levels.

Binding Sites↗
PubMed1977

Isolation and some properties of nontoxigenic derivatives of a strain of Clostridium tetani.

Nontoxigenic derivatives of a toxigenic strain of Clostridium tetani were isolated gy treatment with acridine orange, N-methyl-N'-nitro-soguanidine, rifampicin or ultraviolet light. The frequency of appearance fo non-toxigenic derivatives on these treatments was 0.8 to 3.2 per cent. The nontoxigenic derivatives peoduced all the same extracellular antigenic and protein components as the toxigenic parent strain, except the toxin and materials cross-reacting with the toxin. The nontoxigenic strains, like the toxigenic parent strain, were lyzed by trratment with mitomycin C. Bacteriophage was detected in the lysates of all the nontoxigenic derivatives produced with mitomycin C, and this bacteriophage was morphologically indistinguishable from that obtained from the toxigenic parent strain. The genetic factor controlling tetanus toxin production is discussed.

Antigens, Bacterial↗