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The incompatibility between the PlcR- and AtxA-controlled regulons may have selected a nonsense mutation in Bacillus anthracis.
Mol Microbiol 2001; 42(5):1189-98MM

Abstract

Bacillus anthracis, Bacillus thuringiensis and Bacillus cereus are members of the Bacillus cereus group. These bacteria express virulence in diverse ways in mammals and insects. The pathogenic properties of B. cereus and B. thuringiensis in mammals results largely from the secretion of non-specific toxins, including haemolysins, the production of which depends upon a pleiotropic activator PlcR. In B. anthracis, PlcR is inactive because of a nonsense mutation in the plcR gene. This suggests that the phenotypic differences between B. anthracis on the one hand and B. thuringiensis and B. cereus on the other could result at least partly from loss of the PlcR regulon. We expressed a functional PlcR in B. anthracis. This resulted in the transcriptional activation of genes weakly expressed in the absence of PlcR. The transcriptional activation correlated with the induction of enzymatic activities and toxins including haemolysins. The toxicity of a B. anthracis PlcR+ strain was assayed in the mouse subcutaneous and nasal models of infection. It was no greater than that of the parental strain, suggesting that the PlcR regulon has no influence on B. anthracis virulence. The PlcR regulon had dramatic effects on the sporulation of a B. anthracis strain containing the virulence plasmid pXO1. This resulted from incompatible interactions with the major AtxA-controlled virulence regulon. We propose that the PlcR-controlled regulon in B. anthracis has been counterselected on account of its disadvantageous effects.

Authors+Show Affiliations

Toxines et Pathogénie Bactériennes, Institut Pasteur, 28 rue du Dr Roux, 75724, Paris cédex 15, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11886551

Citation

Mignot, T, et al. "The Incompatibility Between the PlcR- and AtxA-controlled Regulons May Have Selected a Nonsense Mutation in Bacillus Anthracis." Molecular Microbiology, vol. 42, no. 5, 2001, pp. 1189-98.
Mignot T, Mock M, Robichon D, et al. The incompatibility between the PlcR- and AtxA-controlled regulons may have selected a nonsense mutation in Bacillus anthracis. Mol Microbiol. 2001;42(5):1189-98.
Mignot, T., Mock, M., Robichon, D., Landier, A., Lereclus, D., & Fouet, A. (2001). The incompatibility between the PlcR- and AtxA-controlled regulons may have selected a nonsense mutation in Bacillus anthracis. Molecular Microbiology, 42(5), pp. 1189-98.
Mignot T, et al. The Incompatibility Between the PlcR- and AtxA-controlled Regulons May Have Selected a Nonsense Mutation in Bacillus Anthracis. Mol Microbiol. 2001;42(5):1189-98. PubMed PMID: 11886551.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The incompatibility between the PlcR- and AtxA-controlled regulons may have selected a nonsense mutation in Bacillus anthracis. AU - Mignot,T, AU - Mock,M, AU - Robichon,D, AU - Landier,A, AU - Lereclus,D, AU - Fouet,A, PY - 2002/3/12/pubmed PY - 2002/5/8/medline PY - 2002/3/12/entrez SP - 1189 EP - 98 JF - Molecular microbiology JO - Mol. Microbiol. VL - 42 IS - 5 N2 - Bacillus anthracis, Bacillus thuringiensis and Bacillus cereus are members of the Bacillus cereus group. These bacteria express virulence in diverse ways in mammals and insects. The pathogenic properties of B. cereus and B. thuringiensis in mammals results largely from the secretion of non-specific toxins, including haemolysins, the production of which depends upon a pleiotropic activator PlcR. In B. anthracis, PlcR is inactive because of a nonsense mutation in the plcR gene. This suggests that the phenotypic differences between B. anthracis on the one hand and B. thuringiensis and B. cereus on the other could result at least partly from loss of the PlcR regulon. We expressed a functional PlcR in B. anthracis. This resulted in the transcriptional activation of genes weakly expressed in the absence of PlcR. The transcriptional activation correlated with the induction of enzymatic activities and toxins including haemolysins. The toxicity of a B. anthracis PlcR+ strain was assayed in the mouse subcutaneous and nasal models of infection. It was no greater than that of the parental strain, suggesting that the PlcR regulon has no influence on B. anthracis virulence. The PlcR regulon had dramatic effects on the sporulation of a B. anthracis strain containing the virulence plasmid pXO1. This resulted from incompatible interactions with the major AtxA-controlled virulence regulon. We propose that the PlcR-controlled regulon in B. anthracis has been counterselected on account of its disadvantageous effects. SN - 0950-382X UR - https://www.unboundmedicine.com/medline/citation/11886551/The_incompatibility_between_the_PlcR__and_AtxA_controlled_regulons_may_have_selected_a_nonsense_mutation_in_Bacillus_anthracis_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0950-382X&date=2001&volume=42&issue=5&spage=1189 DB - PRIME DP - Unbound Medicine ER -