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Turgor Regulation of Sucrose Transport in Sugar Beet Taproot Tissue

Turgor Regulation of Sucrose Transport in Sugar Beet Taproot Tissue Abstract Sink tissues that store osmotically active compounds must osmoregulate to prevent excessively high turgor. The ability to regulate turgor may be related to membrane transport of solutes and thus sink strength. To study this possibility, the kinetics of sugar uptake were determined in sugar beet (Beta vulgaris L.) taproot tissue discs over a range of cell turgors. Sucrose uptake followed biphasic kinetics with a high affinity saturating component below 20 millimolar and a low affinity linear component at higher concentrations. Glucose uptake exhibited only simple saturation type kinetics. The high affinity saturating component of sucrose and glucose uptake was inhibited by increasing cell turgor (decreasing external mannitol concentrations). The inhibition was evident as a decrease in Vmax but no effect on Km. Sucrose uptake by tissue equilibrated in dilute buffer exhibited no saturating component. Ethylene glycol, a permeant osmoticum, had no effect on uptake kinetics, suggesting that the effect was due to changes in cell turgor and not due to decreased water potential per se. p-(Chloromercuri)benzene sulfonic acid (PCMBS) inhibited sucrose uptake at low but not high cell turgor. High cell turgor caused the tissue to become generally leaky to potassium, sucrose, amino acids, and reducing sugars. PCMBS had no effect on sucrose leakage, an indication that the turgor-induced leakage of sucrose was not via back flow through the carrier. The ability of the tissue to acidify the external media was turgor dependent with an optimum at 300 kilopascals. Acidification was sharply reduced at cell turgors above or below the optimum. The results suggest that the secondary transport of sucrose is reduced at high turgor as a result of inhibition of the plasma membrane ATPase. This inhibition of ATPase activity would explain the reduced Vmax and leakiness to low molecular weight solutes. Cell turgor is an important regulator of sucrose uptake in this tissue and thus may be an important determinant of sink strength in tissues that store sucrose. 2 Current address: United States Department of Agriculture, Agricultural Research Service, Plant Physiology Institute, Tissue Culture and Molecular Biology Laboratory, Room 165-A, Building 011-A, BARC-West, Beltsville, MD 20705. 3 Current address: Department of Agricultural Botany, Faculty of Agriculture, P. O. Box 12, Rehovot 76-100, Israel. 4 Current address: Department of Biochemistry and Soils, University of North Wales, Bangor, Wales. 1 Supported in part by United States Department of Agriculture Grant 82-CRCR-1-1074 Competitive Research Grants Office to R. E. Wyse. Cooperative research of the United States Department of Agriculture, Agricultural Research Service and the Utah Agricultural Experiment Station. Published as Utah Agricultural Experiment Station Journal Article No. 3120. This content is only available as a PDF. © 1986 American Society of Plant Biologists This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Physiology Oxford University Press

Turgor Regulation of Sucrose Transport in Sugar Beet Taproot Tissue

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References (10)

Publisher
Oxford University Press
Copyright
Copyright © 2021 American Society of Plant Biologists
ISSN
0032-0889
eISSN
1532-2548
DOI
10.1104/pp.81.2.478
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Abstract

Abstract Sink tissues that store osmotically active compounds must osmoregulate to prevent excessively high turgor. The ability to regulate turgor may be related to membrane transport of solutes and thus sink strength. To study this possibility, the kinetics of sugar uptake were determined in sugar beet (Beta vulgaris L.) taproot tissue discs over a range of cell turgors. Sucrose uptake followed biphasic kinetics with a high affinity saturating component below 20 millimolar and a low affinity linear component at higher concentrations. Glucose uptake exhibited only simple saturation type kinetics. The high affinity saturating component of sucrose and glucose uptake was inhibited by increasing cell turgor (decreasing external mannitol concentrations). The inhibition was evident as a decrease in Vmax but no effect on Km. Sucrose uptake by tissue equilibrated in dilute buffer exhibited no saturating component. Ethylene glycol, a permeant osmoticum, had no effect on uptake kinetics, suggesting that the effect was due to changes in cell turgor and not due to decreased water potential per se. p-(Chloromercuri)benzene sulfonic acid (PCMBS) inhibited sucrose uptake at low but not high cell turgor. High cell turgor caused the tissue to become generally leaky to potassium, sucrose, amino acids, and reducing sugars. PCMBS had no effect on sucrose leakage, an indication that the turgor-induced leakage of sucrose was not via back flow through the carrier. The ability of the tissue to acidify the external media was turgor dependent with an optimum at 300 kilopascals. Acidification was sharply reduced at cell turgors above or below the optimum. The results suggest that the secondary transport of sucrose is reduced at high turgor as a result of inhibition of the plasma membrane ATPase. This inhibition of ATPase activity would explain the reduced Vmax and leakiness to low molecular weight solutes. Cell turgor is an important regulator of sucrose uptake in this tissue and thus may be an important determinant of sink strength in tissues that store sucrose. 2 Current address: United States Department of Agriculture, Agricultural Research Service, Plant Physiology Institute, Tissue Culture and Molecular Biology Laboratory, Room 165-A, Building 011-A, BARC-West, Beltsville, MD 20705. 3 Current address: Department of Agricultural Botany, Faculty of Agriculture, P. O. Box 12, Rehovot 76-100, Israel. 4 Current address: Department of Biochemistry and Soils, University of North Wales, Bangor, Wales. 1 Supported in part by United States Department of Agriculture Grant 82-CRCR-1-1074 Competitive Research Grants Office to R. E. Wyse. Cooperative research of the United States Department of Agriculture, Agricultural Research Service and the Utah Agricultural Experiment Station. Published as Utah Agricultural Experiment Station Journal Article No. 3120. This content is only available as a PDF. © 1986 American Society of Plant Biologists This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Journal

Plant Physiology – Oxford University Press

Published: Jun 1, 1986

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