In randomly grown tissue culture cells (mouse leukemic lymphoblast, L5178Y) the number, volume, and Na(+) and K(+) content increase as an exponential function with a doubling time of 11.3 hr. In synchronously grown cells the volume increase of the population and of single cells follows the same exponential function as in randomly grown cells. In contrast, the cation content fluctuates during a single cell cycle. About 1(1/2) hr after the cell division burst (at the beginning of the S period), a net loss of K(+) occurs for a period of about 1 hr amounting to about 20% of the total K. Over the next 5 to 6 hr, the deficit in K(+) is eliminated. The Na(+) content shows a double fluctuation. It falls during the cell division burst, rises when the K(+) content decreases, falls again when K(+) content rises, and then increases again before the next cell division burst. The net fluxes of both Na(+) and K(+) are very small compared to the unidirectional fluxes (less than 5%), thus small changes in the balance of influx and efflux account for the changes in cation content during the growth cycle. Both unidirectional fluxes increase dramatically (by a factor of two) about 2 hr after the cell division burst, and then remain constant until after the next cell division. The pattern of electrolyte regulation during cell division does not follow a simple function such as cell number, cell surface, or cell volume, but must be related to specific internal events in the cell.

Animals↗

PubMed1967

Discrimination between alkali metal cations by yeast. II. Cation interactions in transport.

K(+) is a competitive inhibitor of the uptake of the other alkali metal cations by yeast. Rb(+) is a competitive inhibitor of K(+) uptake, but Li(+), Na(+), and Cs(+) act like H(+). At relatively low concentrations they behave as apparent noncompetitive inhibitors of K(+) transport, but the inhibition is incomplete. At higher concentrations they inhibit the remaining K(+) transport competitively. Ca(++) and Mg(++) in relatively low concentrations partially inhibit K(+) transport in an apparently noncompetitive manner although their affinity for the transport site is very low. In each case, in concentrations that produce "noncompetitive" inhibition, very little of the inhibiting cation is transported into the cell. Competitive inhibition is accompanied by appreciable uptake of the inhibiting cation. The apparently noncompetitive effect of other cations is reversed by K(+) concentrations much higher than those necessary to essentially "saturate" the transport system. A model is proposed which can account for the inhibition kinetics. This model is based on two cation-binding sites for which cations compete, a carrier or transporting site, and a second nontransporting (modifier) site with a different array of affinities for cations. The association of certain cations with the modifier site leads to a reduction in the turnover of the carrier, the degree of reduction depending on the cation bound to the modifier site and on the cation being transported.

Biological Transport↗

PubMed1965

Variation K+ and Na+ content during the growth cycle of yeast.

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In Vitro Techniques↗

PubMed1965

Arsenate uptake and release in relation to the inhibition of transport and glycolysis in yeast.

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Acetates↗