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Evidence for a Mechanically Induced Oxidative Burst

Evidence for a Mechanically Induced Oxidative Burst Abstract Rapid release of H2O2 may constitute an initial defense response mounted by a plant. Inauguration of this oxidative burst is known to occur upon stimulation with chemical elicitors, but the possibility of mechanical elicitation arising from pathogen penetration/weakening of the cell wall has never been examined. To introduce an adjustable mechanical stress on the plasma membrane, cultured soybean (Glycine max Merr. cv Kent) cells were subjected to defined changes in medium osmolarity. Dilution of the medium with water or resuspension of cells in sucrose solutions of reduced osmolarity yielded an oxidative burst similar to those stimulated by chemical elicitors. Furthermore, the magnitude of oxidant biosynthesis and osmotic stress correlated directly. Upon return of the cells to normal tonicity, the oxidative burst abruptly halted, indicating that its expression depended on maintenance of the osmotic stress and not on any external chemical signal. To confirm the ability of soybean cells to respond to a mechanical stimulus with induction of an oxidative burst, cells were subjected to direct physical pressure. Application of pressure yielded a characteristic oxidative burst. Because neither these cells nor those subjected to osmotic pressure were damaged by their treatments, we conclude that plant cells can detect mechanical disturbances and initiate a classical defense reaction in response. This content is only available as a PDF. Copyright © 1995 by 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

Evidence for a Mechanically Induced Oxidative Burst

PLANT PHYSIOLOGY , Volume 109 (4) – Dec 1, 1995

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References (40)

Publisher
Oxford University Press
Copyright
Copyright © 2021 American Society of Plant Biologists
ISSN
0032-0889
eISSN
1532-2548
DOI
10.1104/pp.109.4.1259
Publisher site
See Article on Publisher Site

Abstract

Abstract Rapid release of H2O2 may constitute an initial defense response mounted by a plant. Inauguration of this oxidative burst is known to occur upon stimulation with chemical elicitors, but the possibility of mechanical elicitation arising from pathogen penetration/weakening of the cell wall has never been examined. To introduce an adjustable mechanical stress on the plasma membrane, cultured soybean (Glycine max Merr. cv Kent) cells were subjected to defined changes in medium osmolarity. Dilution of the medium with water or resuspension of cells in sucrose solutions of reduced osmolarity yielded an oxidative burst similar to those stimulated by chemical elicitors. Furthermore, the magnitude of oxidant biosynthesis and osmotic stress correlated directly. Upon return of the cells to normal tonicity, the oxidative burst abruptly halted, indicating that its expression depended on maintenance of the osmotic stress and not on any external chemical signal. To confirm the ability of soybean cells to respond to a mechanical stimulus with induction of an oxidative burst, cells were subjected to direct physical pressure. Application of pressure yielded a characteristic oxidative burst. Because neither these cells nor those subjected to osmotic pressure were damaged by their treatments, we conclude that plant cells can detect mechanical disturbances and initiate a classical defense reaction in response. This content is only available as a PDF. Copyright © 1995 by 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 PHYSIOLOGYOxford University Press

Published: Dec 1, 1995

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