Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in Tomato

Plants have evolved sophisticated mechanisms to sense and respond to pathogen attacks. Resistance against necrotrophic pathogens generally requires the activation of the jasmonic acid (JA) signaling pathway, whereas the salicylic acid (SA) signaling pathway is mainly activated against biotrophic pat...

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Autores principales: Rigano, Luciano Ariel, Rodriguez, María Cecilia, Vojnov, Adrian Alberto
Publicado: 2011
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10404651_v23_n6_p2405_ElOirdi
http://hdl.handle.net/20.500.12110/paper_10404651_v23_n6_p2405_ElOirdi
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spelling paper:paper_10404651_v23_n6_p2405_ElOirdi2023-06-08T16:00:48Z Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in Tomato Rigano, Luciano Ariel Rodriguez, María Cecilia Vojnov, Adrian Alberto antiinfective agent cyclopentane derivative defensin glucan jasmonic acid oxylipin salicylic acid vegetable protein article Botrytis chemistry conformation genetics immunology innate immunity metabolism microbiology molecular genetics pathogenicity plant disease plant leaf signal transduction tomato transgenic plant Anti-Infective Agents Botrytis Carbohydrate Conformation Cyclopentanes Defensins Glucans Immunity, Innate Lycopersicon esculentum Molecular Sequence Data Oxylipins Plant Diseases Plant Leaves Plant Proteins Plants, Genetically Modified Salicylic Acid Signal Transduction Botryotinia fuckeliana Fungi Lycopersicon esculentum Plants have evolved sophisticated mechanisms to sense and respond to pathogen attacks. Resistance against necrotrophic pathogens generally requires the activation of the jasmonic acid (JA) signaling pathway, whereas the salicylic acid (SA) signaling pathway is mainly activated against biotrophic pathogens. SA can antagonize JA signaling and vice versa. Here, we report that the necrotrophic pathogen Botrytis cinerea exploits this antagonism as a strategy to cause disease development. We show that B. cinerea produces an exopolysaccharide, which acts as an elicitor of the SA pathway. In turn, the SA pathway antagonizes the JA signaling pathway, thereby allowing the fungus to develop its disease in tomato (Solanum lycopersicum). SA-promoted disease development occurs through Nonexpressed Pathogen Related1. We also show that the JA signaling pathway required for tomato resistance against B. cinerea is mediated by the systemin elicitor. These data highlight a new strategy used by B. cinerea to overcome the plant's defense system and to spread within the host. © 2011 American Society of Plant Biologists. All rights reserved. Fil:Rigano, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Rodriguez, M.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Vojnov, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2011 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10404651_v23_n6_p2405_ElOirdi http://hdl.handle.net/20.500.12110/paper_10404651_v23_n6_p2405_ElOirdi
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic antiinfective agent
cyclopentane derivative
defensin
glucan
jasmonic acid
oxylipin
salicylic acid
vegetable protein
article
Botrytis
chemistry
conformation
genetics
immunology
innate immunity
metabolism
microbiology
molecular genetics
pathogenicity
plant disease
plant leaf
signal transduction
tomato
transgenic plant
Anti-Infective Agents
Botrytis
Carbohydrate Conformation
Cyclopentanes
Defensins
Glucans
Immunity, Innate
Lycopersicon esculentum
Molecular Sequence Data
Oxylipins
Plant Diseases
Plant Leaves
Plant Proteins
Plants, Genetically Modified
Salicylic Acid
Signal Transduction
Botryotinia fuckeliana
Fungi
Lycopersicon esculentum
spellingShingle antiinfective agent
cyclopentane derivative
defensin
glucan
jasmonic acid
oxylipin
salicylic acid
vegetable protein
article
Botrytis
chemistry
conformation
genetics
immunology
innate immunity
metabolism
microbiology
molecular genetics
pathogenicity
plant disease
plant leaf
signal transduction
tomato
transgenic plant
Anti-Infective Agents
Botrytis
Carbohydrate Conformation
Cyclopentanes
Defensins
Glucans
Immunity, Innate
Lycopersicon esculentum
Molecular Sequence Data
Oxylipins
Plant Diseases
Plant Leaves
Plant Proteins
Plants, Genetically Modified
Salicylic Acid
Signal Transduction
Botryotinia fuckeliana
Fungi
Lycopersicon esculentum
Rigano, Luciano Ariel
Rodriguez, María Cecilia
Vojnov, Adrian Alberto
Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in Tomato
topic_facet antiinfective agent
cyclopentane derivative
defensin
glucan
jasmonic acid
oxylipin
salicylic acid
vegetable protein
article
Botrytis
chemistry
conformation
genetics
immunology
innate immunity
metabolism
microbiology
molecular genetics
pathogenicity
plant disease
plant leaf
signal transduction
tomato
transgenic plant
Anti-Infective Agents
Botrytis
Carbohydrate Conformation
Cyclopentanes
Defensins
Glucans
Immunity, Innate
Lycopersicon esculentum
Molecular Sequence Data
Oxylipins
Plant Diseases
Plant Leaves
Plant Proteins
Plants, Genetically Modified
Salicylic Acid
Signal Transduction
Botryotinia fuckeliana
Fungi
Lycopersicon esculentum
description Plants have evolved sophisticated mechanisms to sense and respond to pathogen attacks. Resistance against necrotrophic pathogens generally requires the activation of the jasmonic acid (JA) signaling pathway, whereas the salicylic acid (SA) signaling pathway is mainly activated against biotrophic pathogens. SA can antagonize JA signaling and vice versa. Here, we report that the necrotrophic pathogen Botrytis cinerea exploits this antagonism as a strategy to cause disease development. We show that B. cinerea produces an exopolysaccharide, which acts as an elicitor of the SA pathway. In turn, the SA pathway antagonizes the JA signaling pathway, thereby allowing the fungus to develop its disease in tomato (Solanum lycopersicum). SA-promoted disease development occurs through Nonexpressed Pathogen Related1. We also show that the JA signaling pathway required for tomato resistance against B. cinerea is mediated by the systemin elicitor. These data highlight a new strategy used by B. cinerea to overcome the plant's defense system and to spread within the host. © 2011 American Society of Plant Biologists. All rights reserved.
author Rigano, Luciano Ariel
Rodriguez, María Cecilia
Vojnov, Adrian Alberto
author_facet Rigano, Luciano Ariel
Rodriguez, María Cecilia
Vojnov, Adrian Alberto
author_sort Rigano, Luciano Ariel
title Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in Tomato
title_short Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in Tomato
title_full Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in Tomato
title_fullStr Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in Tomato
title_full_unstemmed Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in Tomato
title_sort botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in tomato
publishDate 2011
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10404651_v23_n6_p2405_ElOirdi
http://hdl.handle.net/20.500.12110/paper_10404651_v23_n6_p2405_ElOirdi
work_keys_str_mv AT riganolucianoariel botrytiscinereamanipulatestheantagonisticeffectsbetweenimmunepathwaystopromotediseasedevelopmentintomato
AT rodriguezmariacecilia botrytiscinereamanipulatestheantagonisticeffectsbetweenimmunepathwaystopromotediseasedevelopmentintomato
AT vojnovadrianalberto botrytiscinereamanipulatestheantagonisticeffectsbetweenimmunepathwaystopromotediseasedevelopmentintomato
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