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Plant Cell Advance Online Publication
Published on April 25, 2008; 10.1105/tpc.108.058362

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Received January 28, 2008
Returned for revision March 31, 2008
Accepted April 9, 2008

Reduced V-ATPase Activity in the trans-Golgi Network Causes Oxylipin-Dependent Hypocotyl Growth Inhibition in Arabidopsis

Angela Brüx 1, Tzu-Yin Liu 1, Melanie Krebs 1, York-Dieter Stierhof 1, Jan U. Lohmann 2, Otto Miersch 3, Claus Wasternack 3, and Karin Schumacher 4*

1 Center for Plant Molecular Biology, University of Tübingen, 72076 Tübingen, Germany
2 Department of Molecular Biology, Max-Planck-Institute for Developmental Biology, 72076 Tübingen, Germany; Center for Organismal Studies, University of Heidelberg, 69120 Heidelberg, Germany
3 Department of Natural Product Biotechnology, Leibniz-Institute of Plant Biochemistry, D-06120 Halle (Saale), Germany
4 Center for Plant Molecular Biology, University of Tübingen, 72076 Tübingen, Germany; Heidelberg Institute of Plant Sciences, University of Heidelberg, 69120 Heidelberg, Germany

* To whom correspondence should be addressed. E-mail: karin.schumacher{at}hip.uni-heidelberg.de.

Regulated cell expansion allows plants to adapt their morphogenesis to prevailing environmental conditions. Cell expansion is driven by turgor pressure created by osmotic water uptake and is restricted by the extensibility of the cell wall, which in turn is regulated by the synthesis, incorporation, and cross-linking of new cell wall components. The vacuolar H+-ATPase (V-ATPase) could provide a way to coordinately regulate turgor pressure and cell wall synthesis, as it energizes the secondary active transport of solutes across the tonoplast and also has an important function in the trans-Golgi network (TGN), which affects synthesis and trafficking of cell wall components. We have previously shown that det3, a mutant with reduced V-ATPase activity, has a severe defect in cell expansion. However, it was not clear if this is caused by a defect in turgor pressure or in cell wall synthesis. Here, we show that inhibition of the tonoplast-localized V-ATPase subunit isoform VHA-a3 does not impair cell expansion. By contrast, inhibition of the TGN-localized isoform VHA-a1 is sufficient to restrict cell expansion. Furthermore, we provide evidence that the reduced hypocotyl cell expansion in det3 is conditional and due to active, hormone-mediated growth inhibition caused by a cell wall defect.




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