Reduced V-ATPase activity in the trans-Golgi network causes Oxylipin-Dependent Hypocotyl growth inhibition in Arabidopsis

• Verfasst von: Brüx, Angela [VerfasserIn]
• Verfasst von: Lohmann, Jan U. [VerfasserIn]
• Verfasst von: Schumacher, Karin [VerfasserIn]
• Titel: Reduced V-ATPase activity in the trans-Golgi network causes Oxylipin-Dependent Hypocotyl growth inhibition in Arabidopsis
• Verf.angabe: Angela Brüx, Tzu-Yin Liu, Melanie Krebs, York-Dieter Stierhof, Jan U. Lohmann, Otto Miersch, Claus Wasternack, and Karin Schumacher
• Umfang: 13 S.
• Fussnoten: Gesehen am 09.05.2017
• Titel Quelle: Enthalten in: The plant cell
• Jahr Quelle: 2008
• Band/Heft Quelle: 20(2008), 4, S. 1088-1100
• ISSN Quelle: 1532-298X
• DOI: doi:10.1105/tpc.108.058362
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1558342583

Abstract

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. Plant architecture, a collection of genetically controlled agronomic traits, is one of the decisive factors that determine grain production. IDEAL PLANT ARCHITECTURE1 (IPA1) encodes a key transcription factor with pleiotropic effects on regulating plant architecture in rice (Oryza sativa), and IPA1 expression is controlled at the posttranscriptional level by microRNA156 and microRNA529. Here, we report the identification and characterization of IPA1 INTERACTING PROTEIN1 (IPI1), a RING-finger E3 ligase that can interact with IPA1 in the nucleus. IPI1 promotes the degradation of IPA1 in panicles, while it stabilizes IPA1 in shoot apexes. Consistent with these findings, the ipi1 loss-of-function mutants showed markedly altered plant architecture, including more tillers, enlarged panicles, and increased yield per plant. Moreover, IPI1 could ubiquitinate the IPA1-mediated complex with different polyubiquitin chains, adding K48-linked polyubiquitin chains in panicles and K63-linked polyubiquitin chains in the shoot apex. These results demonstrate that IPI1 affects plant architecture through precisely tuning IPA1 protein levels in different tissues in rice and provide new insight into the tissue-specific regulation of plant architecture and important genetic resources for molecular breeding.