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  The Nematode Resistance Allele at the rhg1 Locus Alters the Proteome and Primary Metabolism of Soybean Roots

Afzal, A. J., Natarajan, A., Saini, N., Iqbal, M. J., Geisler, M., El Shemy, H. A., et al. (2009). The Nematode Resistance Allele at the rhg1 Locus Alters the Proteome and Primary Metabolism of Soybean Roots. Plant Physiology, 151(3), 1264-1280. doi:10.1104/pp.109.138149.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0014-2649-C Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0014-264A-A
Genre: Journal Article

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Afzal-2009-The Nematode Resista.pdf (Any fulltext), 3MB
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 Creators:
Afzal, A. J.1, Author
Natarajan, A.1, Author
Saini, N.1, Author
Iqbal, M. J.1, Author
Geisler, M.1, Author
El Shemy, H. A.1, Author
Mungur, R.2, 3, Author              
Willmitzer, L.2, Author              
Lightfoot, D. A.1, Author
Affiliations:
1External Organizations, ou_persistent22              
2Small Molecules, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society, ou_1753340              
3Micro- and Protein-Analysis, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society, ou_1753346              

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Free keywords: 2-dimensional gel-electrophoresis capture microdissection lcm kunitz trypsin-inhibitor expressed sequence tags cyst-nematode disease resistance heterodera-glycines gene-expression plant defense mass-spectrometry
 Abstract: Heterodera glycines, the soybean cyst nematode (SCN), causes the most damaging chronic disease of soybean (Glycine max). Host resistance requires the resistance allele at rhg1. Resistance destroys the giant cells created in the plant's roots by the nematodes about 24 to 48 h after commencement of feeding. In addition, 4 to 8 d later, a systemic acquired resistance develops that discourages later infestations. The molecular mechanisms that control the rhg1-mediated resistance response appear to be multigenic and complex, as judged by transcript abundance changes, even in near isogenic lines (NILs). This study aimed to focus on key posttranscriptional changes by identifying proteins and metabolites that were increased in abundance in both resistant and susceptible NILs. Comparisons were made among NILs 10 d after SCN infestation and without SCN infestation. Two-dimensional gel electrophoresis resolved more than 1,000 protein spots on each gel. Only 30 protein spots with a significant (P < 0.05) difference in abundance of 1.5-fold or more were found among the four treatments. The proteins in these spots were picked, trypsin digested, and analyzed using quadrupole time-of-flight tandem mass spectrometry. Protein identifications could be made for 24 of the 30 spots. Four spots contained two proteins, so that 28 distinct proteins were identified. The proteins were grouped into six functional categories. Metabolite analysis by gas chromatography-mass spectrometry identified 131 metabolites, among which 58 were altered by one or more treatment; 28 were involved in primary metabolism. Taken together, the data showed that 17 pathways were altered by the rhg1 alleles. Pathways altered were associated with systemic acquired resistance-like responses, including xenobiotic, phytoalexin, ascorbate, and inositol metabolism, as well as primary metabolisms like amino acid synthesis and glycolysis. The pathways impacted by the rhg1 allelic state and SCN infestation agreed with transcript abundance analyses but identified a smaller set of key proteins. Six of the proteins lay within the same small region of the interactome identifying a key set of 159 interacting proteins involved in transcriptional control, nuclear localization, and protein degradation. Finally, two proteins (glucose-6-phosphate isomerase [EC 5.3.1.9] and isoflavone reductase [EC 1.3.1.45]) and two metabolites (maltose and an unknown) differed in resistant and susceptible NILs without SCN infestation and may form the basis of a new assay for the selection of resistance to SCN in soybean.

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Language(s): eng - English
 Dates: 2009-05-122009
 Publication Status: Published in print
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 Table of Contents: -
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 Identifiers: ISI: ISI:000271430500029
DOI: 10.1104/pp.109.138149
ISSN: 1532-2548 (Electronic) 0032-0889 (Linking)
URI: ://000271430500029 http://www.jstor.org/stable/pdfplus/40537952.pdf
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Title: Plant Physiology
Source Genre: Journal
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Pages: - Volume / Issue: 151 (3) Sequence Number: - Start / End Page: 1264 - 1280 Identifier: -