6533b830fe1ef96bd12967ed
RESEARCH PRODUCT
Variant toxin B and a functional toxin A produced by Clostridium difficile C34.
Veit BraunDavid E. MahonyMichael MoosChristoph Von Eichel-streiberMarkus MehligBettina Kaltsubject
MaleCell SurvivalBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BGTPaseEnterotoxinCHO CellsBiologymedicine.disease_causeMicrobiologyMicrobiologyEnterotoxinsBacterial ProteinsCricetinaeGeneticsmedicineAnimalsHumansMolecular BiologyCells CulturedCytopathic effectSkinToxinClostridioides difficileCytotoxinsGenetic VariationClostridium difficileMolecular biologyCdc42 GTP-Binding ProteinDNA Transposable ElementsMicroscopy Electron Scanningdescription
A particular property of Clostridium difficile strain C34 is an insertion of approximately 2 kb in the tcdA-C34 gene that does not hinder expression of a fully active TcdA-C34 molecule. Intoxication with TcdA-C34 induced an arborized appearance in eukaryotic cells (D-type cytopathic effect); intoxication with TcdB-C34 induced a spindle-like appearance of cells (S-type cytopathic effect). Inactivation of GTPases with purified toxins revealed that Rho, Rac, Cdc42, and Rap are substrates of TcdA-C34. The variant cytotoxin TcdB-C34 inactivated Rho, Rac, Cdc42, Rap, Ral, and R-Ras. Hence, this is the first ‘S-type’ cytotoxin which inactivates both Rho and R-Ras, and is coexpressed with a ‘D-type’ enterotoxin. Our results support the hypothesis that R-Ras is a key GTPase related to the S-type cytopathic effect and suggest that induction of a S-type cytopathic effect dominates induction of the D-type cytopathic effect.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2001-05-01 | FEMS microbiology letters |