Contrasting Regulation of NO and ROS in Potato Defense-Associated Metabolism in Response to Pathogens of Different Lifestyles.
Identifieur interne : 000C79 ( Main/Exploration ); précédent : 000C78; suivant : 000C80Contrasting Regulation of NO and ROS in Potato Defense-Associated Metabolism in Response to Pathogens of Different Lifestyles.
Auteurs : Jolanta Floryszak-Wieczorek [Pologne] ; Magdalena Arasimowicz-Jelonek [Pologne]Source :
- PloS one [ 1932-6203 ] ; 2016.
Descripteurs français
- KwdFr :
- Botrytis (métabolisme), Botrytis (pathogénicité), Espèces réactives de l'oxygène (métabolisme), Feuilles de plante (microbiologie), Feuilles de plante (métabolisme), Glycoprotéines (métabolisme), Génotype (MeSH), Maladies des plantes (génétique), Maladies des plantes (microbiologie), Monoxyde d'azote (métabolisme), Mort cellulaire (MeSH), Oxydoréduction (MeSH), Peroxyde d'hydrogène (composition chimique), Phytophthora infestans (métabolisme), Phytophthora infestans (pathogénicité), Protéines d'Arabidopsis (MeSH), Protéines végétales (métabolisme), Régulation de l'expression des gènes végétaux (MeSH), Résistance à la maladie (génétique), Solanum tuberosum (microbiologie), Solanum tuberosum (métabolisme), Superoxydes (métabolisme).
- MESH :
- composition chimique : Peroxyde d'hydrogène.
- génétique : Maladies des plantes, Résistance à la maladie.
- microbiologie : Feuilles de plante, Maladies des plantes, Solanum tuberosum.
- métabolisme : Botrytis, Espèces réactives de l'oxygène, Feuilles de plante, Glycoprotéines, Monoxyde d'azote, Phytophthora infestans, Protéines végétales, Solanum tuberosum, Superoxydes.
- pathogénicité : Botrytis, Phytophthora infestans.
- Génotype, Mort cellulaire, Oxydoréduction, Protéines d'Arabidopsis, Régulation de l'expression des gènes végétaux.
English descriptors
- KwdEn :
- Arabidopsis Proteins (MeSH), Botrytis (metabolism), Botrytis (pathogenicity), Cell Death (MeSH), Disease Resistance (genetics), Gene Expression Regulation, Plant (MeSH), Genotype (MeSH), Glycoproteins (metabolism), Hydrogen Peroxide (chemistry), Nitric Oxide (metabolism), Oxidation-Reduction (MeSH), Phytophthora infestans (metabolism), Phytophthora infestans (pathogenicity), Plant Diseases (genetics), Plant Diseases (microbiology), Plant Leaves (metabolism), Plant Leaves (microbiology), Plant Proteins (metabolism), Reactive Oxygen Species (metabolism), Solanum tuberosum (metabolism), Solanum tuberosum (microbiology), Superoxides (metabolism).
- MESH :
- chemical , chemistry : Hydrogen Peroxide.
- chemical , metabolism : Glycoproteins, Nitric Oxide, Plant Proteins, Reactive Oxygen Species, Superoxides.
- chemical : Arabidopsis Proteins.
- genetics : Disease Resistance, Plant Diseases.
- metabolism : Botrytis, Phytophthora infestans, Plant Leaves, Solanum tuberosum.
- microbiology : Plant Diseases, Plant Leaves, Solanum tuberosum.
- pathogenicity : Botrytis, Phytophthora infestans.
- Cell Death, Gene Expression Regulation, Plant, Genotype, Oxidation-Reduction.
Abstract
Our research provides new insights into how the low and steady-state levels of nitric oxide (NO) and reactive oxygen species (ROS) in potato leaves are altered after the challenge with the hemibiotroph Phytophthora infestans or the necrotroph Botrytis cinerea, with the subsequent rapid and invader-dependent modification of defense responses with opposite effects. Mainly in the avirulent (avr) P. infestans-potato system, NO well balanced with the superoxide level was tuned with a battery of SA-dependent defense genes, leading to the establishment of the hypersensitive response (HR) successfully arresting the pathogen. Relatively high levels of S-nitrosoglutathione and S-nitrosothiols concentrated in the main vein of potato leaves indicated the mobile function of these compounds as a reservoir of NO bioactivity. In contrast, low-level production of NO and ROS during virulent (vr) P. infestans-potato interactions might be crucial in the delayed up-regulation of PR-1 and PR-3 genes and compromised resistance to the hemibiotrophic pathogen. In turn, B. cinerea triggered huge NO overproduction and governed inhibition of superoxide production by blunting NADPH oxidase. Nevertheless, a relatively high level of H2O2 was found owing to the germin-like activity in cooperation with NO-mediated HR-like cell death in potato genotypes favorable to the necrotrophic pathogen. Moreover, B. cinerea not only provoked cell death, but also modulated the host redox milieu by boosting protein nitration, which attenuated SA production but not SA-dependent defense gene expression. Finally, based on obtained data the organismal cost of having machinery for HR in plant resistance to biotrophs is also discussed, while emphasizing new efforts to identify other components of the NO/ROS cell death pathway and improve plant protection against pathogens of different lifestyles.
DOI: 10.1371/journal.pone.0163546
PubMed: 27695047
PubMed Central: PMC5047594
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Mainly in the avirulent (avr) P. infestans-potato system, NO well balanced with the superoxide level was tuned with a battery of SA-dependent defense genes, leading to the establishment of the hypersensitive response (HR) successfully arresting the pathogen. Relatively high levels of S-nitrosoglutathione and S-nitrosothiols concentrated in the main vein of potato leaves indicated the mobile function of these compounds as a reservoir of NO bioactivity. In contrast, low-level production of NO and ROS during virulent (vr) P. infestans-potato interactions might be crucial in the delayed up-regulation of PR-1 and PR-3 genes and compromised resistance to the hemibiotrophic pathogen. In turn, B. cinerea triggered huge NO overproduction and governed inhibition of superoxide production by blunting NADPH oxidase. Nevertheless, a relatively high level of H2O2 was found owing to the germin-like activity in cooperation with NO-mediated HR-like cell death in potato genotypes favorable to the necrotrophic pathogen. Moreover, B. cinerea not only provoked cell death, but also modulated the host redox milieu by boosting protein nitration, which attenuated SA production but not SA-dependent defense gene expression. Finally, based on obtained data the organismal cost of having machinery for HR in plant resistance to biotrophs is also discussed, while emphasizing new efforts to identify other components of the NO/ROS cell death pathway and improve plant protection against pathogens of different lifestyles.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27695047</PMID><DateCompleted><Year>2017</Year><Month>06</Month><Day>27</Day></DateCompleted><DateRevised><Year>2019</Year><Month>02</Month><Day>12</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>10</Issue><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Contrasting Regulation of NO and ROS in Potato Defense-Associated Metabolism in Response to Pathogens of Different Lifestyles.</ArticleTitle><Pagination><MedlinePgn>e0163546</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0163546</ELocationID><Abstract><AbstractText>Our research provides new insights into how the low and steady-state levels of nitric oxide (NO) and reactive oxygen species (ROS) in potato leaves are altered after the challenge with the hemibiotroph Phytophthora infestans or the necrotroph Botrytis cinerea, with the subsequent rapid and invader-dependent modification of defense responses with opposite effects. Mainly in the avirulent (avr) P. infestans-potato system, NO well balanced with the superoxide level was tuned with a battery of SA-dependent defense genes, leading to the establishment of the hypersensitive response (HR) successfully arresting the pathogen. Relatively high levels of S-nitrosoglutathione and S-nitrosothiols concentrated in the main vein of potato leaves indicated the mobile function of these compounds as a reservoir of NO bioactivity. In contrast, low-level production of NO and ROS during virulent (vr) P. infestans-potato interactions might be crucial in the delayed up-regulation of PR-1 and PR-3 genes and compromised resistance to the hemibiotrophic pathogen. In turn, B. cinerea triggered huge NO overproduction and governed inhibition of superoxide production by blunting NADPH oxidase. Nevertheless, a relatively high level of H2O2 was found owing to the germin-like activity in cooperation with NO-mediated HR-like cell death in potato genotypes favorable to the necrotrophic pathogen. Moreover, B. cinerea not only provoked cell death, but also modulated the host redox milieu by boosting protein nitration, which attenuated SA production but not SA-dependent defense gene expression. Finally, based on obtained data the organismal cost of having machinery for HR in plant resistance to biotrophs is also discussed, while emphasizing new efforts to identify other components of the NO/ROS cell death pathway and improve plant protection against pathogens of different lifestyles.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Floryszak-Wieczorek</LastName><ForeName>Jolanta</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Plant Physiology, Poznan University of Life Sciences, Wolynska 35, 60-637 Poznan, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arasimowicz-Jelonek</LastName><ForeName>Magdalena</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Plant Ecophysiology, Faculty of Biology, Adam Mickiewicz University, Umultowska 89, 61-614 Poznan, Poland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>10</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029681">Arabidopsis Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006023">Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010940">Plant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>11062-77-4</RegistryNumber><NameOfSubstance UI="D013481">Superoxides</NameOfSubstance></Chemical><Chemical><RegistryNumber>123339-15-1</RegistryNumber><NameOfSubstance UI="C058814">germin</NameOfSubstance></Chemical><Chemical><RegistryNumber>147445-32-7</RegistryNumber><NameOfSubstance UI="C077262">PR-1 protein, Arabidopsis</NameOfSubstance></Chemical><Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber><NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D029681" MajorTopicYN="N">Arabidopsis Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020171" MajorTopicYN="N">Botrytis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D060467" MajorTopicYN="N">Disease Resistance</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018506" MajorTopicYN="N">Gene Expression Regulation, Plant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006023" MajorTopicYN="N">Glycoproteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055750" MajorTopicYN="N">Phytophthora infestans</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018515" MajorTopicYN="N">Plant Leaves</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010940" MajorTopicYN="N">Plant Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011198" MajorTopicYN="N">Solanum tuberosum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013481" MajorTopicYN="N">Superoxides</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>07</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>09</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>10</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>10</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27695047</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0163546</ArticleId><ArticleId IdType="pii">PONE-D-16-29725</ArticleId><ArticleId IdType="pmc">PMC5047594</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Biochem J. 2012 Oct 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