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  Perturbation of Arabidopsis Amino Acid Metabolism Causes Incompatibility with the Adapted Biotrophic Pathogen Hyaloperonospora arabidopsidis

Stuttmann, J., Hubberten, H.-M., Rietz, S., Kaur, J., Muskett, P., Guerois, R., et al. (2011). Perturbation of Arabidopsis Amino Acid Metabolism Causes Incompatibility with the Adapted Biotrophic Pathogen Hyaloperonospora arabidopsidis. Plant Cell, 23(7), 2788-2803. doi:10.1105/tpc.111.087684.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0014-20B0-3 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0014-20B1-1
Genre: Journal Article

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 Creators:
Stuttmann, J.1, Author
Hubberten, H.-M.2, Author              
Rietz, S.1, Author
Kaur, J.1, Author
Muskett, P.1, Author
Guerois, R.1, Author
Bednarek, P.1, Author
Hoefgen, R.2, Author              
Parker, J. E.1, Author
Affiliations:
1External Organizations, ou_persistent22              
2Amino Acid and Sulfur Metabolism, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society, ou_1753337              

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Free keywords: cystathionine gamma-synthase downy mildew resistance disease resistance aspartate kinase peronospora-parasitica salicylic-acid powdery mildew dihydrodipicolinate synthase lysine biosynthesis signaling pathways
 Abstract: Reliance of biotrophic pathogens on living plant tissues to propagate implies strong interdependence between host metabolism and nutrient uptake by the pathogen. However, factors determining host suitability and establishment of infection are largely unknown. We describe a loss-of-inhibition allele of ASPARTATE KINASE2 and a loss-of-function allele of DIHYDRODIPICOLINATE SYNTHASE2 identified in a screen for Arabidopsis thaliana mutants with increased resistance to the obligate biotrophic oomycete Hyaloperonospora arabidopsidis (Hpa). Through different molecular mechanisms, these mutations perturb amino acid homeostasis leading to overaccumulation of the Asp-derived amino acids Met, Thr, and Ile. Although detrimental for the plant, the mutations do not cause defense activation, and both mutants retain full susceptibility to the adapted obligate biotrophic fungus Golovinomyces orontii (Go). Chemical treatments mimicking the mutants' metabolic state identified Thr as the amino acid suppressing Hpa but not Go colonization. We conclude that perturbations in amino acid homeostasis render the mutant plants unsuitable as an infection substrate for Hpa. This may be explained by deployment of the same amino acid biosynthetic pathways by oomycetes and plants. Our data show that the plant host metabolic state can, in specific ways, influence the ability of adapted biotrophic strains to cause disease.

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Language(s): eng - English
 Dates: 2011-07-222011
 Publication Status: Published in print
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 Identifiers: ISI: ISI:000294164300028
DOI: 10.1105/tpc.111.087684
ISSN: 1040-4651
URI: ://000294164300028 http://www.plantcell.org/content/23/7/2788.full.pdf
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Title: Plant Cell
Source Genre: Journal
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Pages: - Volume / Issue: 23 (7) Sequence Number: - Start / End Page: 2788 - 2803 Identifier: -