Intracellular signal triggered by cholera toxin in Saccharomyces boulardii and Saccharomyces cerevisiae.
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1998
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As is the case for Saccharomyces boulardii, Saccharomyces cerevisiae W303 protects Fisher rats against cholera
toxin (CT). The addition of glucose or dinitrophenol to cells of S. boulardii grown on a nonfermentable carbon
source activated trehalase in a manner similar to that observed for S. cerevisiae. The addition of CT to the same
cells also resulted in trehalase activation. Experiments performed separately on the A and B subunits of CT
showed that both are necessary for activation. Similarly, the addition of CT but not of its separate subunits led
to a cyclic AMP (cAMP) signal in both S. boulardii and S. cerevisiae. These data suggest that trehalase
stimulation by CT probably occurred through the cAMP-mediated protein phosphorylation cascade. The
requirement of CT subunit B for both the cAMP signal and trehalase activation indicates the presence of a
specific receptor on the yeasts able to bind to the toxin, a situation similar to that observed for mammalian
cells. This hypothesis was reinforced by experiments with 125I-labeled CT showing specific binding of the toxin
to yeast cells. The adhesion of CT to a receptor on the yeast surface through the B subunit and internalization
of the A subunit (necessary for the cAMP signal and trehalase activation) could be one more mechanism
explaining protection against the toxin observed for rats treated with yeasts.
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BRANDÃO, R. L. et al. Intracellular signal triggered by cholera toxin in Saccharomyces boulardii and Saccharomyces cerevisiae. Applied and Environmental Microbiology, v. 642, p. 564-568, 1998. Disponível em: <http://aem.asm.org/content/64/2/564.long> Acesso em: 10 jan. 2017