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First published online September 20, 2002; 10.1104/pp.006064

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Plant Physiol, October 2002, Vol. 130, pp. 895-903

A Comparison of Oligogalacturonide- and Auxin-Induced Extracellular Alkalinization and Growth Responses in Roots of Intact Cucumber Seedlings1

Mark D. Spiro,* Jonathan F. Bowers, and Daniel J. Cosgrove

Biology Department, Bucknell University, Lewisburg, Pennsylvania 17837 (M.D.S., J.F.B.); and Root Biology Program and Department of Biology, The Pennsylvania State University, University Park, Pennsylvania 16802 (M.D.S., D.J.C.)

Oligogalacturonic acid (OGA) affects plant growth and development in an antagonistic manner to that of the auxin indole-3-acetic acid (IAA), the mechanism by which remains to be determined. This study describes the relationship between IAA and OGA activity in intact cucumber (Cucumis sativus) seedlings. Both OGA and IAA induced rapid and transient extracellular alkalinization; however, the characteristics of the OGA and IAA responses differed in their kinetics, magnitude, calcium dependence, and region of the root in which they induced their maximal response. IAA (1 µM) induced a saturating alkalinization response of approximately 0.2 pH unit and a rapid reduction (approximately 80%) in root growth that only partially recovered over 20 h. OGAs, specifically those with a degree of polymerization of 10 to 13, induced a maximal alkalinization response of 0.48 pH unit, but OGA treatment did not alter root growth. Saturating concentrations of OGA did not block IAA-induced alkalinization or the initial IAA-induced inhibition of root growth but allowed IAA-treated roots to recover their initial growth rate within 270 min. IAA-induced alkalinization occurs primarily in the growing apical region of the root, whereas OGA induced its maximal response in the basal region of the root. This study demonstrates that OGA and IAA act by distinct mechanisms and that OGA does not simply act by inhibition of IAA action. These results also suggest that IAA-induced extracellular alkalinization is not sufficient to account for the mechanism by which IAA inhibits root growth.


1 This work was supported in part by the Root Biology Training Program at the Pennsylvania State University, a unit of the Department of Energy/National Science Foundation/U.S. Department of Agriculture Collaborative Research Program in Plant Biology, and in part by the Department of Energy (grant no. DE-FG02-84ER13179).

* Corresponding author; e-mail spiro{at}bucknell.edu; fax 570- 577-3537.

© 2002 American Society of Plant Physiologists



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