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Cytolethal Distending Toxin Subunit B: A Review of Structure-Function Relationship.

Authors
  • Pons, Benoît J1, 2
  • Vignard, Julien3
  • Mirey, Gladys4
  • 1 Toxalim (Research Centre in Food Toxicology), Université de Toulouse, INRA, ENVT, INP-Purpan, UPS, 31300 Toulouse, France. [email protected] , (France)
  • 2 Research Centre in Food Toxicology, Université Toulouse III-Paul Sabatier (UPS), 31400 Toulouse, France. [email protected] , (France)
  • 3 Toxalim (Research Centre in Food Toxicology), Université de Toulouse, INRA, ENVT, INP-Purpan, UPS, 31300 Toulouse, France. [email protected] , (France)
  • 4 Toxalim (Research Centre in Food Toxicology), Université de Toulouse, INRA, ENVT, INP-Purpan, UPS, 31300 Toulouse, France. [email protected] , (France)
Type
Published Article
Journal
Toxins
Publisher
MDPI AG
Publication Date
Oct 12, 2019
Volume
11
Issue
10
Identifiers
DOI: 10.3390/toxins11100595
PMID: 31614800
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The Cytolethal Distending Toxin (CDT) is a bacterial virulence factor produced by several Gram-negative pathogenic bacteria. These bacteria, found in distinct niches, cause diverse infectious diseases and produce CDTs differing in sequence and structure. CDTs have been involved in the pathogenicity of the associated bacteria by promoting persistent infection. At the host-cell level, CDTs cause cell distension, cell cycle block and DNA damage, eventually leading to cell death. All these effects are attributable to the catalytic CdtB subunit, but its exact mode of action is only beginning to be unraveled. Sequence and 3D structure analyses revealed similarities with better characterized proteins, such as nucleases or phosphatases, and it has been hypothesized that CdtB exerts a biochemical activity close to those enzymes. Here, we review the relationships that have been established between CdtB structure and function, particularly by mutation experiments on predicted key residues in different experimental systems. We discuss the relevance of these approaches and underline the importance of further study in the molecular mechanisms of CDT toxicity, particularly in the context of different pathological conditions.

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