INTRACELLULAR SIGNAL TRIGGERED BY CHOLERA-TOXIN IN SACCHAROMYCES-BOULARDII AND SACCHAROMYCES-CEREVISIAE

As is the case for Saccharomyces boulardii, Saccharomyces cerevisiae W 303 protects Fisher rats against cholera toxin (CT). The addition of g lucose or dinitrophenol to cells of S. boulardii grown on a nonferment able carbon source activated trehalase in a manner similar to that obs erved for S. cerevisiae. The addition of CT to the same cells also res ulted 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. Th ese data suggest that trehalase stimulation by CT probably occurred th rough the cAMP-mediated protein phosphorylation cascade. The requireme nt of CT subunit B for both the cAMP signal and trehalase activation i ndicates the presence of a specific receptor on the yeasts able to bin d to the toxin, a situation similar to that observed for mammalian cel ls, This hypothesis was reinforced by experiments with I-125-labeled C T showing specific binding of the toxin to yeast cells. The adhesion o f CT to a receptor on the yeast surface through the B subunit and inte rnalization of the A subunit (necessary for the cAMP signal and trehal ase activation) could be one more mechanism explaining protection agai nst the toxin observed for rats treated with yeasts.