Alkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to Botrytis cinerea in Arabidopsis thaliana.

Alkamides are fatty acid amides of wide distribution in plants, structurally related to N-acyl-L-homoserine lactones (AHLs) from Gram-negative bacteria and to N- acylethanolamines (NAEs) from plants and mammals. Global analysis of gene expression changes in Arabidopsis thaliana in response to N-isob...

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Autores principales: Alfonso Méndez-Bravo, Carlos Calderón-Vázquez, Enrique Ibarra-Laclette, Javier Raya-González, Enrique Ramírez-Chávez, Jorge Molina-Torres, Angel A Guevara-García, José López-Bucio, Luis Herrera-Estrella
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Publicado: Public Library of Science (PLoS) 2011
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spelling oai:doaj.org-article:e16e92386e7442219ff2ec674744d6fc2021-11-18T07:34:55ZAlkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to Botrytis cinerea in Arabidopsis thaliana.1932-620310.1371/journal.pone.0027251https://doaj.org/article/e16e92386e7442219ff2ec674744d6fc2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22076141/?tool=EBIhttps://doaj.org/toc/1932-6203Alkamides are fatty acid amides of wide distribution in plants, structurally related to N-acyl-L-homoserine lactones (AHLs) from Gram-negative bacteria and to N- acylethanolamines (NAEs) from plants and mammals. Global analysis of gene expression changes in Arabidopsis thaliana in response to N-isobutyl decanamide, the most highly active alkamide identified to date, revealed an overrepresentation of defense-responsive transcriptional networks. In particular, genes encoding enzymes for jasmonic acid (JA) biosynthesis increased their expression, which occurred in parallel with JA, nitric oxide (NO) and H₂O₂ accumulation. The activity of the alkamide to confer resistance against the necrotizing fungus Botrytis cinerea was tested by inoculating Arabidopsis detached leaves with conidiospores and evaluating disease symptoms and fungal proliferation. N-isobutyl decanamide application significantly reduced necrosis caused by the pathogen and inhibited fungal proliferation. Arabidopsis mutants jar1 and coi1 altered in JA signaling and a MAP kinase mutant (mpk6), unlike salicylic acid- (SA) related mutant eds16/sid2-1, were unable to defend from fungal attack even when N-isobutyl decanamide was supplied, indicating that alkamides could modulate some necrotrophic-associated defense responses through JA-dependent and MPK6-regulated signaling pathways. Our results suggest a role of alkamides in plant immunity induction.Alfonso Méndez-BravoCarlos Calderón-VázquezEnrique Ibarra-LacletteJavier Raya-GonzálezEnrique Ramírez-ChávezJorge Molina-TorresAngel A Guevara-GarcíaJosé López-BucioLuis Herrera-EstrellaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 11, p e27251 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Alfonso Méndez-Bravo
Carlos Calderón-Vázquez
Enrique Ibarra-Laclette
Javier Raya-González
Enrique Ramírez-Chávez
Jorge Molina-Torres
Angel A Guevara-García
José López-Bucio
Luis Herrera-Estrella
Alkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to Botrytis cinerea in Arabidopsis thaliana.
description Alkamides are fatty acid amides of wide distribution in plants, structurally related to N-acyl-L-homoserine lactones (AHLs) from Gram-negative bacteria and to N- acylethanolamines (NAEs) from plants and mammals. Global analysis of gene expression changes in Arabidopsis thaliana in response to N-isobutyl decanamide, the most highly active alkamide identified to date, revealed an overrepresentation of defense-responsive transcriptional networks. In particular, genes encoding enzymes for jasmonic acid (JA) biosynthesis increased their expression, which occurred in parallel with JA, nitric oxide (NO) and H₂O₂ accumulation. The activity of the alkamide to confer resistance against the necrotizing fungus Botrytis cinerea was tested by inoculating Arabidopsis detached leaves with conidiospores and evaluating disease symptoms and fungal proliferation. N-isobutyl decanamide application significantly reduced necrosis caused by the pathogen and inhibited fungal proliferation. Arabidopsis mutants jar1 and coi1 altered in JA signaling and a MAP kinase mutant (mpk6), unlike salicylic acid- (SA) related mutant eds16/sid2-1, were unable to defend from fungal attack even when N-isobutyl decanamide was supplied, indicating that alkamides could modulate some necrotrophic-associated defense responses through JA-dependent and MPK6-regulated signaling pathways. Our results suggest a role of alkamides in plant immunity induction.
format article
author Alfonso Méndez-Bravo
Carlos Calderón-Vázquez
Enrique Ibarra-Laclette
Javier Raya-González
Enrique Ramírez-Chávez
Jorge Molina-Torres
Angel A Guevara-García
José López-Bucio
Luis Herrera-Estrella
author_facet Alfonso Méndez-Bravo
Carlos Calderón-Vázquez
Enrique Ibarra-Laclette
Javier Raya-González
Enrique Ramírez-Chávez
Jorge Molina-Torres
Angel A Guevara-García
José López-Bucio
Luis Herrera-Estrella
author_sort Alfonso Méndez-Bravo
title Alkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to Botrytis cinerea in Arabidopsis thaliana.
title_short Alkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to Botrytis cinerea in Arabidopsis thaliana.
title_full Alkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to Botrytis cinerea in Arabidopsis thaliana.
title_fullStr Alkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to Botrytis cinerea in Arabidopsis thaliana.
title_full_unstemmed Alkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to Botrytis cinerea in Arabidopsis thaliana.
title_sort alkamides activate jasmonic acid biosynthesis and signaling pathways and confer resistance to botrytis cinerea in arabidopsis thaliana.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/e16e92386e7442219ff2ec674744d6fc
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