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Sporulation and Sporulation-Associated Toxin Production

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  • Authors: Jihong Li1, Daniel Paredes-Sabja2, Mahfuzur R. Sarker3, Bruce A. McClane4
  • Editors: Patrick Eichenberger5, Adam Driks6
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219; 2: Departamento de Ciencias Biológicas, Universidad Andrés Bello, Santiago, 920-8640, Chile; 3: Department of Biomedical Sciences, College of Veterinary Medicine, Department of Microbiology, College of Science, Oregon State University, Corvallis, OR 15219; 4: Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219; 5: New York University, New York, NY; 6: Loyola University Medical Center, Maywood, IL
  • Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.TBS-0022-2015
  • Received 10 November 2015 Accepted 10 November 2015 Published 13 May 2016
  • Bruce A. McClane, bamcc@pitt.edu
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  • Abstract:

    The ability of to form spores plays a key role during the transmission of this Gram-positive bacterium to cause disease. Of particular note, the spores produced by food poisoning strains are often exceptionally resistant to food environment stresses such as heat, cold, and preservatives, which likely facilitates their survival in temperature-abused foods. The exceptional resistance properties of spores made by most type A food poisoning strains and some type C foodborne disease strains involve their production of a variant small acid-soluble protein-4 that binds more tightly to spore DNA than to the small acid-soluble protein-4 made by most other strains. Sporulation and germination by and spp. share both similarities and differences. Finally, sporulation is essential for production of enterotoxin, which is responsible for the symptoms of type A food poisoning, the second most common bacterial foodborne disease in the United States. During this foodborne disease, is ingested with food and then, by using sporulation-specific alternate sigma factors, this bacterium sporulates and produces the enterotoxin in the intestines.

  • Citation: Li J, Paredes-Sabja D, Sarker M, McClane B. 2016. Sporulation and Sporulation-Associated Toxin Production. Microbiol Spectrum 4(3):TBS-0022-2015. doi:10.1128/microbiolspec.TBS-0022-2015.

Key Concept Ranking

Multilocus Sequence Typing
0.42081907
Mobile Genetic Elements
0.40852576
0.42081907

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/content/journal/microbiolspec/10.1128/microbiolspec.TBS-0022-2015
2016-05-13
2017-03-25

Abstract:

The ability of to form spores plays a key role during the transmission of this Gram-positive bacterium to cause disease. Of particular note, the spores produced by food poisoning strains are often exceptionally resistant to food environment stresses such as heat, cold, and preservatives, which likely facilitates their survival in temperature-abused foods. The exceptional resistance properties of spores made by most type A food poisoning strains and some type C foodborne disease strains involve their production of a variant small acid-soluble protein-4 that binds more tightly to spore DNA than to the small acid-soluble protein-4 made by most other strains. Sporulation and germination by and spp. share both similarities and differences. Finally, sporulation is essential for production of enterotoxin, which is responsible for the symptoms of type A food poisoning, the second most common bacterial foodborne disease in the United States. During this foodborne disease, is ingested with food and then, by using sporulation-specific alternate sigma factors, this bacterium sporulates and produces the enterotoxin in the intestines.

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Figures

Image of FIGURE 1
FIGURE 1

Ultrastructure of spores. Transmission electron micrograph of a spore from strain H-6, a food poisoning strain. Components of spore shown include proteinaceous spore coat layers, the cortex region, and the core with ribosomes giving a granular appearance. The bar represents 1.0 µM. Reproduced with permission from reference 9 . doi:10.1128/microbiolspec.TBS-0022-2015.f1

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.TBS-0022-2015
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Image of FIGURE 2
FIGURE 2

Sporulation-associated sigma factors are required for sporulation. Shown are photomicrographs of sporulating cultures of SM101, a transformable derivative of a food poisoning strain, after growth for 8 h in Duncan-Strong sporulation medium. Also shown is the absence of sporulating cells in similar Duncan-Strong cultures of a or null mutant of SM101 (SM101:: or SM101::). This loss of sporulation was specifically due to inactivation of the or genes in those mutants since the effect was reversible by complementation, i.e., by adding back a wild-type or gene, respectively, to those mutants (SM101::Comp or SM101::Comp). Reproduced with permission from reference 28 . Similar loss of sporulation was observed with or mutants of SM101 ( 29 ). doi:10.1128/microbiolspec.TBS-0022-2015.f2

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.TBS-0022-2015
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Image of FIGURE 3
FIGURE 3

Sporulation in . Working through unidentified intermediates, the Agr QS system and CcpA affect Spo0A expression or, possibly, phosphorylation to initiate sporulation. This triggers a cascade of sigma factors where SigF controls production of the three other sporulation-associated sigma factors. Two of these sigma factors (SigE and SigK) then regulate CPE production during sporulation. Compiled from references 28 , 29 , 31 , and 44 . Not shown in this drawing, SigE (and possibly SigK) can also regulate production of TpeL toxin ( 97 ). doi:10.1128/microbiolspec.TBS-0022-2015.f3

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.TBS-0022-2015
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FIGURE 4

DNA binding properties of recombinant His6-tagged SASP4. (A) Electromobility shift assays (EMSAs) showing binding to biotin-labeled DNA by purified rSASP4 from F4969 (a CPE-positive non-foodborne human GI disease strain that forms sensitive spores and produces an SASP4 variant with a Gly at residue 36), SM101 or 01E809 (two CPE-positive food poisoning isolates that form resistant spores and produce an SASP4 variant with Asp at residue 36). (B) EMSAs showing binding by purified SM101 rSASP4 or rSASP2 to (left) AT-rich biotin-labeled DNA or (right) biotin-labeled GC-rich DNA. Reproduced with permission from references 42 and 78 . doi:10.1128/microbiolspec.TBS-0022-2015.f4

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.TBS-0022-2015
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FIGURE 5

Current model for the mechanism of action of CPE. CPE binds to claudin receptors to form small complexes. Those small complexes then oligomerize on the host cell surface to form an ∼450-kDa prepore known as CH-1. The prepore inserts into the membrane to form an active pore that alters host plasma membrane permeability for small molecules. As a result, calcium enters the cytoplasm and triggers either apoptosis (caused by low CPE doses, where there is a modest calcium influx) or oncosis (caused by high CPE doses, where there is a strong calcium influx). Reproduced with permission from reference 1 . doi:10.1128/microbiolspec.TBS-0022-2015.f5

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.TBS-0022-2015
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