Summary: Caesium accumulation by , from buffer (pH 8.0) supplemented with 50 μM-CsCl and Cs, continued for approximately 15 h and displayed first-order kinetics, indicating a single rate-limiting transport process. Efflux of Cs from Cs-loaded cells occurred in two distinct phases: a rapid initial loss, representing approximately 11% of total cellular Cs, corresponded to release from the cell surface, whereas a second, slower, phase of efflux corresponded to loss from the cytoplasm and vacuole. Analysis of subcellular Cs compartmentation revealed that most Cs was accumulated into the vacuole of , with lesser amounts being associated with the cell surface or located in the cytoplasm. Uptake of Cs into the vacuole was correlated with a stoichiometric exchange for K. However, no loss of K from the cell surface or cytoplasm was evident nor was Cs or K associated with insoluble intracellular components. Calculated values for the Cs flux across the vacuolar membrane were approximately equal to, or higher than, values for total cellular influx. Cs influx obeyed Michaelis–Menten kinetics over the lower range of external Cs concentrations examined (0.01–0.25 mM) and a single transport system with a ± 0.5 mM was evident. The effects of other monovalent cations on Cs influx implied that K and Rb were competitive, and NH non-competitive/uncompetitive inhibitors of Cs uptake. The order of inhibition was Rb > K > NH . We propose that a single, relatively non-selective, rate-limiting transport system for Cs influx is located on the cytoplasmic membrane of , while a more permeable vacuolar membrane facilitates transport of Cs into the vacuole.


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