Lack of the Golgi phosphate transporter PHT4;6 causes strong developmental defects, constitutively activated disease resistance mechanisms and altered intracellular phosphate compartmentation in Arabidopsis
Article first published online: 12 OCT 2012
© 2012 The Authors. The Plant Journal © 2012 Blackwell Publishing Ltd
The Plant Journal
Volume 72, Issue 5, pages 732–744, December 2012
How to Cite
Hassler, S., Lemke, L., Jung, B., Möhlmann, T., Krüger, F., Schumacher, K., Espen, L., Martinoia, E. and Neuhaus, H. E. (2012), Lack of the Golgi phosphate transporter PHT4;6 causes strong developmental defects, constitutively activated disease resistance mechanisms and altered intracellular phosphate compartmentation in Arabidopsis. The Plant Journal, 72: 732–744. doi: 10.1111/j.1365-313X.2012.05106.x
- Issue published online: 22 NOV 2012
- Article first published online: 12 OCT 2012
- Accepted manuscript online: 12 JUL 2012 12:37PM EST
- Received 26 March 2012; revised 29 June 2012; accepted 10 July 2012; published online 12 October 2012.
- inorganic phosphate;
- Golgi apparatus;
- phosphate compartmentation;
- mimic disease;
The Golgi-located phosphate exporter PHT4;6 has been described as involved in salt tolerance but further analysis on the physiological impact of PHT4;6 remained elusive. Here we show that PHT4;6–GFP is targeted to the trans-Golgi compartment and that loss of function of this carrier protein has a dramatic impact on plant growth and development. Knockout mutants of pht4;6 exhibit a dwarf phenotype that is complemented by the homologous gene from rice (Oryza sativa). Interestingly, pht4;6 mutants show altered characteristics of several Golgi-related functions, such as an altered abundance of certain N-glycosylated proteins, altered composition of cell-wall hemicelluose, and higher sensitivity to the Golgi α-mannosidase and the retrograde transport inhibitors kifunensine and brefeldin A, respectively. Moreover, pht4;6 mutants exhibit a ‘mimic disease’ phenotype accompanied by constitutively activated pathogen defense mechanisms and increased resistance against the virulent Pseudomonas syringae strain DC3000. Surprisingly, pht4;6 mutants also exhibit phosphate starvation symptoms, as revealed at the morphological and molecular level, although total Pi levels in wild-type and pht4;6 plants are similar. This suggested that subcellular Pi compartmentation was impaired. By use of nuclear magnetic resonance (NMR), increased Pi concentration was detected in acidic compartments of pht4;6 mutants. We propose that impaired Pi efflux from the trans-Golgi lumen results in accumulation of inorganic phosphate in other internal compartments, leading to low cytoplasmic phosphate levels with detrimental effects on plant performance.