The DinJ/RelE Toxin-Antitoxin System Suppresses Bacterial Proliferation and Virulence of Xylella fastidiosa in Grapevine.
Identifieur interne : 000293 ( Main/Exploration ); précédent : 000292; suivant : 000294The DinJ/RelE Toxin-Antitoxin System Suppresses Bacterial Proliferation and Virulence of Xylella fastidiosa in Grapevine.
Auteurs : Lindsey P. Burbank [États-Unis] ; Drake C. Stenger [États-Unis]Source :
- Phytopathology [ 0031-949X ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Antitoxines (génétique), Antitoxines (métabolisme), Feuilles de plante (microbiologie), Interactions hôte-pathogène (MeSH), Maladies des plantes (immunologie), Maladies des plantes (microbiologie), Opéron (génétique), Protéines bactériennes (génétique), Protéines bactériennes (métabolisme), Régions promotrices (génétique) (génétique), Techniques de knock-out de gènes (MeSH), Toxines bactériennes (génétique), Toxines bactériennes (métabolisme), Vecteurs insectes (microbiologie), Virulence (MeSH), Vitis (immunologie), Vitis (microbiologie), Xylella (croissance et développement), Xylella (génétique), Xylella (pathogénicité), Xylème (microbiologie).
- MESH :
- croissance et développement : Xylella.
- génétique : Antitoxines, Opéron, Protéines bactériennes, Régions promotrices (génétique), Toxines bactériennes, Xylella.
- immunologie : Maladies des plantes, Vitis.
- microbiologie : Feuilles de plante, Maladies des plantes, Vecteurs insectes, Vitis, Xylème.
- métabolisme : Antitoxines, Protéines bactériennes, Toxines bactériennes.
- pathogénicité : Xylella.
- Animaux, Interactions hôte-pathogène, Techniques de knock-out de gènes, Virulence.
English descriptors
- KwdEn :
- Animals (MeSH), Antitoxins (genetics), Antitoxins (metabolism), Bacterial Proteins (genetics), Bacterial Proteins (metabolism), Bacterial Toxins (genetics), Bacterial Toxins (metabolism), Gene Knockout Techniques (MeSH), Host-Pathogen Interactions (MeSH), Insect Vectors (microbiology), Operon (genetics), Plant Diseases (immunology), Plant Diseases (microbiology), Plant Leaves (microbiology), Promoter Regions, Genetic (genetics), Virulence (MeSH), Vitis (immunology), Vitis (microbiology), Xylella (genetics), Xylella (growth & development), Xylella (pathogenicity), Xylem (microbiology).
- MESH :
- chemical , genetics : Antitoxins, Bacterial Proteins, Bacterial Toxins.
- chemical , metabolism : Antitoxins, Bacterial Proteins, Bacterial Toxins.
- genetics : Operon, Promoter Regions, Genetic, Xylella.
- growth & development : Xylella.
- immunology : Plant Diseases, Vitis.
- microbiology : Insect Vectors, Plant Diseases, Plant Leaves, Vitis, Xylem.
- pathogenicity : Xylella.
- Animals, Gene Knockout Techniques, Host-Pathogen Interactions, Virulence.
Abstract
Xylella fastidiosa, the causal agent of Pierce's disease of grapes, is a slow-growing, xylem-limited, bacterial pathogen. Disease progression is characterized by systemic spread of the bacterium through xylem vessel networks, causing leaf-scorching symptoms, senescence, and vine decline. It appears to be advantageous to this pathogen to avoid excessive blockage of xylem vessels, because living bacterial cells are generally found in plant tissue with low bacterial cell density and minimal scorching symptoms. The DinJ/RelE toxin-antitoxin system is characterized here for a role in controlling bacterial proliferation and population size during plant colonization. The DinJ/RelE locus is transcribed from two separate promoters, allowing for coexpression of antitoxin DinJ with endoribonuclease toxin RelE, in addition to independent expression of RelE. The ratio of antitoxin/toxin expressed is dependent on bacterial growth conditions, with lower amounts of antitoxin present under conditions designed to mimic grapevine xylem sap. A knockout mutant of DinJ/RelE exhibits a hypervirulent phenotype, with higher bacterial populations and increased symptom development and plant decline. It is likely that DinJ/RelE acts to prevent excessive population growth, contributing to the ability of the pathogen to spread systemically without completely blocking the xylem vessels and increasing probability of acquisition by the insect vector.
DOI: 10.1094/PHYTO-10-16-0374-R
PubMed: 27938243
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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type="abstract" xml:lang="en">Xylella fastidiosa, the causal agent of Pierce's disease of grapes, is a slow-growing, xylem-limited, bacterial pathogen. Disease progression is characterized by systemic spread of the bacterium through xylem vessel networks, causing leaf-scorching symptoms, senescence, and vine decline. It appears to be advantageous to this pathogen to avoid excessive blockage of xylem vessels, because living bacterial cells are generally found in plant tissue with low bacterial cell density and minimal scorching symptoms. The DinJ/RelE toxin-antitoxin system is characterized here for a role in controlling bacterial proliferation and population size during plant colonization. The DinJ/RelE locus is transcribed from two separate promoters, allowing for coexpression of antitoxin DinJ with endoribonuclease toxin RelE, in addition to independent expression of RelE. The ratio of antitoxin/toxin expressed is dependent on bacterial growth conditions, with lower amounts of antitoxin present under conditions designed to mimic grapevine xylem sap. A knockout mutant of DinJ/RelE exhibits a hypervirulent phenotype, with higher bacterial populations and increased symptom development and plant decline. It is likely that DinJ/RelE acts to prevent excessive population growth, contributing to the ability of the pathogen to spread systemically without completely blocking the xylem vessels and increasing probability of acquisition by the insect vector.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27938243</PMID><DateCompleted><Year>2017</Year><Month>07</Month><Day>20</Day></DateCompleted><DateRevised><Year>2017</Year><Month>07</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0031-949X</ISSN><JournalIssue CitedMedium="Print"><Volume>107</Volume><Issue>4</Issue><PubDate><Year>2017</Year><Month>04</Month></PubDate></JournalIssue><Title>Phytopathology</Title><ISOAbbreviation>Phytopathology</ISOAbbreviation></Journal><ArticleTitle>The DinJ/RelE Toxin-Antitoxin System Suppresses Bacterial Proliferation and Virulence of Xylella fastidiosa in Grapevine.</ArticleTitle><Pagination><MedlinePgn>388-394</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1094/PHYTO-10-16-0374-R</ELocationID><Abstract><AbstractText>Xylella fastidiosa, the causal agent of Pierce's disease of grapes, is a slow-growing, xylem-limited, bacterial pathogen. Disease progression is characterized by systemic spread of the bacterium through xylem vessel networks, causing leaf-scorching symptoms, senescence, and vine decline. It appears to be advantageous to this pathogen to avoid excessive blockage of xylem vessels, because living bacterial cells are generally found in plant tissue with low bacterial cell density and minimal scorching symptoms. The DinJ/RelE toxin-antitoxin system is characterized here for a role in controlling bacterial proliferation and population size during plant colonization. The DinJ/RelE locus is transcribed from two separate promoters, allowing for coexpression of antitoxin DinJ with endoribonuclease toxin RelE, in addition to independent expression of RelE. The ratio of antitoxin/toxin expressed is dependent on bacterial growth conditions, with lower amounts of antitoxin present under conditions designed to mimic grapevine xylem sap. A knockout mutant of DinJ/RelE exhibits a hypervirulent phenotype, with higher bacterial populations and increased symptom development and plant decline. It is likely that DinJ/RelE acts to prevent excessive population growth, contributing to the ability of the pathogen to spread systemically without completely blocking the xylem vessels and increasing probability of acquisition by the insect vector.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Burbank</LastName><ForeName>Lindsey P</ForeName><Initials>LP</Initials><AffiliationInfo><Affiliation>United States Department of Agriculture-Agricultural Research Service, San Joaquin Valley Agricultural Sciences Center, Parlier, CA 93648-9757.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stenger</LastName><ForeName>Drake C</ForeName><Initials>DC</Initials><AffiliationInfo><Affiliation>United States Department of Agriculture-Agricultural Research Service, San Joaquin Valley Agricultural Sciences Center, Parlier, CA 93648-9757.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Phytopathology</MedlineTA><NlmUniqueID>9427222</NlmUniqueID><ISSNLinking>0031-949X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000992">Antitoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001427">Bacterial Toxins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000992" MajorTopicYN="N">Antitoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001427" MajorTopicYN="N">Bacterial Toxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055786" MajorTopicYN="N">Gene Knockout Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007303" MajorTopicYN="N">Insect Vectors</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009876" MajorTopicYN="N">Operon</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018515" MajorTopicYN="N">Plant Leaves</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D027843" MajorTopicYN="N">Vitis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044167" MajorTopicYN="N">Xylella</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052584" MajorTopicYN="N">Xylem</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>12</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>7</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>12</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27938243</ArticleId><ArticleId IdType="doi">10.1094/PHYTO-10-16-0374-R</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Burbank, Lindsey P" sort="Burbank, Lindsey P" uniqKey="Burbank L" first="Lindsey P" last="Burbank">Lindsey P. Burbank</name></region><name sortKey="Stenger, Drake C" sort="Stenger, Drake C" uniqKey="Stenger D" first="Drake C" last="Stenger">Drake C. Stenger</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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