The response of P220, a salt-tolerant strain of soybean rhizobia, to osmotic shock was investigated by using non-growing washed cells. Rapid changes in K, Mg, glutamate and homospermidine were observed in strain P220 cells subjected to sudden changes in the osmolarity of incubation buffer. Osmotic upshock resulted in elevation of cellular K and glutamate, and reduction in cellular homospermidine and Mg. When the cells were transferred to upshock buffer lacking K, the reduction in Mg was totally blocked, but the elevation of glutamate and the reduction in homospermidine were only partially repressed. Osmotic downshock resulted in the opposite phenomenon: There was an elevation of homospermidine and Mg, and a rapid fall of K and glutamate. When the cells were transferred to downshock buffer lacking Mg, the elevation of homospermidine was partially repressed, but the decrease in K and glutamate was not repressed at all. Lowering of the cellular K by treatment with ionophores nigericin and monensin resulted in a slight decrease in glutamate and a slight increase in homospermidine and Mg, possibly due to a pH effect caused by the K-H exchange. Raising the cellular Mg content by treatment with ionophore A23187 brought about an increase in homospermidine. The homospermidine content of Mg-deficient cells grown with low-Mg medium reduced to 35% of those grown with the basal medium. These results indicate that in , K strictly controls Mg flux during osmotic shock whereas the reverse is not true, and that glutamate and homospermidine essentially escape direct control by K. We also suggest that Mg, which has no effect on the pool size of glutamate, is one of the factors which regulate homospermidine content in rhizobial cells.


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