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Resolution of quantitative resistance to clubroot into QTL-specific metabolic modules

Plant disease resistance is often under quantitative genetic control. Thus, in a given interaction, plant cellular responses to infection are influenced by resistance or susceptibility alleles at different loci. In this study, a genetic linkage analysis was used to address the complexity of the meta...

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Autores principales: Wagner, Geoffrey, Laperche, Anne, Lariagon, Christine, Marnet, Nathalie, Renault, David, Guitton, Yann, Bouchereau, Alain, Delourme, Régine, Manzanares-Dauleux, Maria J, Gravot, Antoine
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6793449/
https://www.ncbi.nlm.nih.gov/pubmed/31145785
http://dx.doi.org/10.1093/jxb/erz265
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author Wagner, Geoffrey
Laperche, Anne
Lariagon, Christine
Marnet, Nathalie
Renault, David
Guitton, Yann
Bouchereau, Alain
Delourme, Régine
Manzanares-Dauleux, Maria J
Gravot, Antoine
author_facet Wagner, Geoffrey
Laperche, Anne
Lariagon, Christine
Marnet, Nathalie
Renault, David
Guitton, Yann
Bouchereau, Alain
Delourme, Régine
Manzanares-Dauleux, Maria J
Gravot, Antoine
author_sort Wagner, Geoffrey
collection PubMed
description Plant disease resistance is often under quantitative genetic control. Thus, in a given interaction, plant cellular responses to infection are influenced by resistance or susceptibility alleles at different loci. In this study, a genetic linkage analysis was used to address the complexity of the metabolic responses of Brassica napus roots to infection by Plasmodiophora brassicae. Metabolome profiling and pathogen quantification in a segregating progeny allowed a comparative mapping of quantitative trait loci (QTLs) involved in resistance and in metabolic adjustments. Distinct metabolic modules were associated with each resistance QTL, suggesting the involvement of different underlying cellular mechanisms. This approach highlighted the possible role of gluconasturtiin and two unknown metabolites in the resistance conferred by two QTLs on chromosomes C03 and C09, respectively. Only two susceptibility biomarkers (glycine and glutathione) were simultaneously linked to the three main resistance QTLs, suggesting the central role of these compounds in the interaction. By contrast, several genotype-specific metabolic responses to infection were genetically unconnected to resistance or susceptibility. Likewise, variations of root sugar profiles, which might have influenced pathogen nutrition, were not found to be related to resistance QTLs. This work illustrates how genetic metabolomics can help to understand plant stress responses and their possible links with disease.
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spelling pubmed-67934492019-10-18 Resolution of quantitative resistance to clubroot into QTL-specific metabolic modules Wagner, Geoffrey Laperche, Anne Lariagon, Christine Marnet, Nathalie Renault, David Guitton, Yann Bouchereau, Alain Delourme, Régine Manzanares-Dauleux, Maria J Gravot, Antoine J Exp Bot Research Papers Plant disease resistance is often under quantitative genetic control. Thus, in a given interaction, plant cellular responses to infection are influenced by resistance or susceptibility alleles at different loci. In this study, a genetic linkage analysis was used to address the complexity of the metabolic responses of Brassica napus roots to infection by Plasmodiophora brassicae. Metabolome profiling and pathogen quantification in a segregating progeny allowed a comparative mapping of quantitative trait loci (QTLs) involved in resistance and in metabolic adjustments. Distinct metabolic modules were associated with each resistance QTL, suggesting the involvement of different underlying cellular mechanisms. This approach highlighted the possible role of gluconasturtiin and two unknown metabolites in the resistance conferred by two QTLs on chromosomes C03 and C09, respectively. Only two susceptibility biomarkers (glycine and glutathione) were simultaneously linked to the three main resistance QTLs, suggesting the central role of these compounds in the interaction. By contrast, several genotype-specific metabolic responses to infection were genetically unconnected to resistance or susceptibility. Likewise, variations of root sugar profiles, which might have influenced pathogen nutrition, were not found to be related to resistance QTLs. This work illustrates how genetic metabolomics can help to understand plant stress responses and their possible links with disease. Oxford University Press 2019-10-01 2019-05-30 /pmc/articles/PMC6793449/ /pubmed/31145785 http://dx.doi.org/10.1093/jxb/erz265 Text en © The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Experimental Biology. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Research Papers
Wagner, Geoffrey
Laperche, Anne
Lariagon, Christine
Marnet, Nathalie
Renault, David
Guitton, Yann
Bouchereau, Alain
Delourme, Régine
Manzanares-Dauleux, Maria J
Gravot, Antoine
Resolution of quantitative resistance to clubroot into QTL-specific metabolic modules
title Resolution of quantitative resistance to clubroot into QTL-specific metabolic modules
title_full Resolution of quantitative resistance to clubroot into QTL-specific metabolic modules
title_fullStr Resolution of quantitative resistance to clubroot into QTL-specific metabolic modules
title_full_unstemmed Resolution of quantitative resistance to clubroot into QTL-specific metabolic modules
title_short Resolution of quantitative resistance to clubroot into QTL-specific metabolic modules
title_sort resolution of quantitative resistance to clubroot into qtl-specific metabolic modules
topic Research Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6793449/
https://www.ncbi.nlm.nih.gov/pubmed/31145785
http://dx.doi.org/10.1093/jxb/erz265
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