Ethylene synthesis and growth of tomato hypocotyls: Induction by auxin and fusicoccin and inhibition by vanadate |
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Authors: | Maureen O Kelly and Kent J Bradford |
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Institution: | (1) Department of Vegetable Crops, University of California, 95616 Davis, California, USA;(2) Present address: Section of Plant Biology, Cornell University, 14853 Ithaca, New York, USA |
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Abstract: | The effects of fusicoccin (FC) on growth and ethylene synthesis of tomato (Lycopersicon esculentum Mill.) hypocotyls were compared to those of indole-3-acetic acid (IAA). Fusicoccin promoted both growth and ethylene production maximally at <2 M. Growth was stimulated to a slightly greater extent by FC as compared to IAA, while ethylene synthesis rates in response to FC were about 50% less than those induced by IAA. Cycloheximide (0.5 M) inhibited auxin-induced growth by 80% but had no effect on FC-induced growth; ethylene production was inhibited to the same extent (58%) when induced by either IAA or FC. Both IAA and FC caused tissue contents of 1-aminocyclopropane-1-carboxylic acid (ACC) and malonyl-ACC to increase, indicating that like IAA, FC induces ethylene synthesis by stimulating the formation of ACC. Orthovanadate, a potent inhibitor of proton-translocating plasma membrane ATPases, reduced both IAA- and FC-induced growth and ethylene synthesis at concentrations less than 1 mM, with ethylene synthesis being approximately 10 times more sensitive to inhibition than growth. Vanadate did not affect tissue ACC levels, slightly reduced total ACC production, and inhibited conversion of ACC to ethylene. However, significant inhibition of in vivo ethylene-forming enzyme activity required high concentrations of vanadate (1 mM) and was less effective than inhibition by cobaltous ion. The site of action of vanadate in inhibiting ethylene synthesis remains unclear, but the ion did not prevent the elevation of tissue ACC levels in response to IAA or FC. It is unlikely, therefore, that stimulation of plasma membrane H+-ATPase activity is required for the induction of ACC synthase by IAA and FC. |
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