Plant Physiology Preview
Published on October 3, 2002; 10.1104/pp.004564
Received February 20, 2002
Returned for revision March 22, 2002
Accepted June 10, 2002
The KNAT2 Homeodomain Protein Interacts with Ethylene and Cytokinin Signaling
Olivier Hamant , Fabien Nogué , Enric Belles-Boix , Delphine Jublot , Olivier Grandjean , Jan Traas , and Véronique Pautot *
Laboratoire de Biologie Cellulaire (O.H., E.B.-B., D.J., J.T., V.P.) and Station de Génétique et d'Amélioration des Plantes (F.N., O.G.), Institut National de la Recherche Agronomique, Route de St. Cyr, 78026 Versailles cedex, France
* Corresponding author; email: pautot{at}versailles.inra.fr.
Using a transgenic line that overexpresses a fusion of the KNAT2 (KNOTTED-like Arabidopsis) homeodomain protein and the hormone-binding domain of the glucocorticoid receptor (GR), we have investigated the possible relations between KNAT2 and various hormones. Upon activation of the KNAT2-GR fusion, we observed a delayed senescence of the leaves and a higher rate of shoot initiation, two processes that are also induced by cytokinins and inhibited by ethylene. Furthermore, the activation of the KNAT2-GR fusion induced lobing of the leaves. This feature was partially suppressed by treatment with the ethylene precursor 1-aminocyclopropane-1-carboxylic acid, or by the constitutive ethylene response ctr1 mutation. Conversely, some phenotypic traits of the ctr1 mutant were suppressed by the activation of the KNAT2-GR fusion. These data suggest that KNAT2 acts synergistically with cytokinins and antagonistically with ethylene. In the shoot apical meristem, the KNAT2 gene is expressed in the L3 layer and the rib zone. 1-Aminocyclopropane-1-carboxylic acid treatment restricted the KNAT2 expression domain in the shoot apical meristem and reduced the number of cells in the L3. The latter effect was suppressed by the activation of the KNAT2-GR construct. Conversely, the KNAT2 gene expression domain was enlarged in the ethylene-resistant etr1-1 mutant or in response to cytokinin treatment. These data suggest that ethylene and cytokinins act antagonistically in the meristem via KNAT2 to regulate the meristem activity.
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