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 morphogenesisto prevailing environmental conditions. Cell expansion is drivenby turgor pressure created by osmotic water uptake and is restrictedby the extensibility of the cell wall, which in turn is regulatedby the synthesis, incorporation, and cross-linking of new cellwall components. The vacuolar H⁺-ATPase (V-ATPase) could providea way to coordinately regulate turgor pressure and cell wallsynthesis, as it energizes the secondary active transport ofsolutes across the tonoplast and also has an important functionin the trans-Golgi network (TGN), which affects synthesis andtrafficking of cell wall components. We have previously shownthat det3, a mutant with reduced V-ATPase activity, has a severedefect in cell expansion. However, it was not clear if thisis caused by a defect in turgor pressure or in cell wall synthesis.Here, we show that inhibition of the tonoplast-localized V-ATPasesubunit isoform VHA-a3 does not impair cell expansion. By contrast,inhibition of the TGN-localized isoform VHA-a1 is sufficientto restrict cell expansion. Furthermore, we provide evidencethat the reduced hypocotyl cell expansion in det3 is conditionaland due to active, hormone-mediated growth inhibition causedby a cell wall defect.