Carrier-Mediated ABA Uptake by Suspension-CulturedPhaseolus coccineusL. Cells: Stereospecificity and Inhibition by Ionones and ABA Esters

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Abstract
Astle, M. and Rubery, P. 1987. Carrier-mediated ABA uptake by suspension-cultured Phaseolus coccineus L. cells: Stereospecificity and inhibition by ionones and ABA esters.—J. exp. Bot. 38: 150–163. The substrate for the abscisic acid (ABA) carrier in Phaseolus coccineus L. suspension-cultured cells is shown to be the (S)ABA enantiomer, Km = 1·0 mmol m–3. The methyl (MeABA) and phenyl (PheABA) esters of ABA inhibit carrier-mediated uptake of ABA with half-maximal inhibition achieved at about 7·0 mmol m–3 and 10 mmol m–3 respectively: with (S)MeABA this value is decreased to about 2·0 mmol m–3. There is no demethylation of radioactive MeABA by the cells during 5 min incubations. Although MeABA reversibly inhibits the ABA carrier, it is not a transport substrate: association of radioactive MeABA with living cells is unaffected by non-radioactive MeABA or ABA and, by comparison with frozen-and-thawed cells, it is shown that the radioactivity remains extracellular. It is proposed that MeABA binds to the carrier to form an abortive complex that is not translocated. The terpenoid ABA analogue LAB 144143 also inhibits carrier-mediated ABA uptake. At concentrations up to about 20 mmol m–3 α- and β-ionone specifically inhibit the ABA carrier with the half-maximal effect at about 0·6 mmol m–3 β-ionone. However, at higher ionone concentrations, the uptake of ABA, indol-3-yl acetic acid and of 5,5-dimethyloxazolidine-2,4-dione (DMO) are all stimulated: this may reflect general permeabilization of the membrane to weak acids by ionone.