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Prevention of the cytopathic effect induced by Clostridium difficile Toxin B by active Rac1
Author(s) -
Halabi-Cabezon Ismael,
Huelsenbeck Johannes,
May Martin,
Ladwein Markus,
Rottner Klemens,
Just Ingo,
Genth Harald
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.10.003
Subject(s) - rhoa , clostridium difficile toxin b , clostridium difficile toxin a , rac1 , transfection , shigella flexneri , pore forming toxin , chemistry , biology , microbiology and biotechnology , clostridium difficile , cell culture , toxin , biochemistry , escherichia coli , signal transduction , microbial toxins , genetics , gene , antibiotics
Clostridium difficile Toxin B (TcdB) glucosylates low molecular weight GTP‐binding proteins of the Rho subfamily and thereby causes actin re‐organization (cell rounding). This “cytopathic effect” has been generally attributed to RhoA inactivation. Here we show that cells expressing non‐glucosylatable Rac1‐Q61L are protected from the cytopathic effect of TcdB. In contrast, cells expressing RhoA‐Q63L or mock‐transfected cells are fully susceptible for the cytopathic effect of TcdB. These findings are extended to the Rac1/RhoG mimic IpgB1 and the RhoA mimic IpgB2 from Shigella . Ectopic expression of IpgB1, but not IpgB2, counteracts the cytopathic effect of TcdB. These data strongly suggest that Rac1 rather than RhoA glucosylation is critical for the cytopathic effect of TcdB.