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Plant Cell, Vol. 10, 713-720, May 1998, Copyright © 1998, American Society of Plant Physiologists
Asymmetric Responsiveness to Ethylene Mediates Cell Elongation in the Apical Hook of Peas
Scott C. Pecka,
Katharina Pawlowskib, and
Hans Kendea
a Michigan State University–Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824-1312
b Department of Molecular Biology, Agricultural University, 6703 HA Wageningen, The Netherlands
Correspondence to:
Hans Kende, hkende{at}pilot.msu.edu (E-mail), 517-353-9168 (fax).
The apical hook of dark-grown dicotyledonous seedlings is a protective structure resulting from an inhibition of cell elongation on the inner portion of the hook. This differential growth response is mediated by ethylene. Expression of the gene encoding 1-aminocyclopropane-1-carboxylate oxidase (ACO), the terminal enzyme in ethylene biosynthesis, is induced by ethylene via a positive feedback loop. Therefore, the ACO transcript can serve as a molecular marker for both ethylene formation and ethylene responsiveness. We examined the distribution of ACO mRNA of pea, Ps-ACO1, and of ACO enzyme activity in the apical hook of etiolated pea seedlings. In situ hybridization showed that cells on the inner, concave side of pea hooks accumulated more Ps-ACO1 mRNA than did cells on the outer, convex side. The distribution of ACO enzyme activity followed the same pattern. A direct correlation was observed between the cellular distribution of Ps-ACO1 mRNA, ACO enzyme activity, and the inhibition of cell elongation. Pea seedlings treated with a saturating concentration of ethylene still accumulated higher levels of the Ps-ACO1 transcript on the inner side of the apical hook, demonstrating an increased responsiveness to ethylene in this tissue. These results indicate that an asymmetrically distributed component of the ethylene signal transduction pathway mediates hook formation. Based on existing genetic evidence, we propose that this component is downstream from the serine/threonine protein kinase CTR1.
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