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 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.
Plant Physiology, University of Kaiserslautern, Erwin Schrödinger Straße, D-67653 Kaiserslautern, Germany.
Sebastian
S
Hassler
Lilia
L
Lemke
Benjamin
B
Jung
Torsten
T
Möhlmann
Falco
F
Krüger
Karin
K
Schumacher
Luca
L
Espen
Enrico
E
Martinoia
H Ekkehard
HE
Neuhaus
D000470:Alkaloids / Q000494:pharmacology; D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000254:growth & development / Q000378:metabolism* / Q000382:microbiology; D029681:Arabidopsis Proteins / Q000235:genetics* / Q000378:metabolism; D020126:Brefeldin A / Q000494:pharmacology; D002473:Cell Wall / Q000737:chemistry; D060467:Disease Resistance; D055785:Gene Knockdown Techniques; D005816:Genetic Complementation Test; D006056:Golgi Apparatus / Q000235:genetics / Q000378:metabolism*; D009154:Mutation; D012275:Oryza / Q000235:genetics; D028061:Phosphate Transport Proteins / Q000235:genetics* / Q000378:metabolism; D010935:Plant Diseases / Q000382:microbiology; D030821:Plants, Genetically Modified; D011134:Polysaccharides / Q000378:metabolism; D044224:Pseudomonas syringae / Q000472:pathogenicity; D043323:alpha-Mannosidase / Q000378:metabolism
D000470:Alkaloids; D029681:Arabidopsis Proteins; C580850:PHT4;6 protein, Arabidopsis; D028061:Phosphate Transport Proteins; D011134:Polysaccharides; C065629:kifunensine; D020126:Brefeldin A; C007916:hemicellulose; D043323:alpha-Mannosidase