Rapid genetic change underpins antagonistic coevolution in a natural host-pathogen metapopulation.
Identifieur interne : 000092 ( Main/Exploration ); précédent : 000091; suivant : 000093Rapid genetic change underpins antagonistic coevolution in a natural host-pathogen metapopulation.
Auteurs : Peter H. Thrall [Australie] ; Anna-Liisa Laine ; Michael Ravensdale ; Adnane Nemri ; Peter N. Dodds ; Luke G. Barrett ; Jeremy J. BurdonSource :
- Ecology letters [ 1461-0248 ] ; 2012.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Basidiomycota, Lin, Résistance à la maladie.
- microbiologie : Lin.
- pathogénicité : Basidiomycota.
- physiologie : Basidiomycota.
- Génotype, Interactions hôte-parasite, Variation génétique, Évolution biologique.
English descriptors
- KwdEn :
- MESH :
- genetics : Basidiomycota, Disease Resistance, Flax.
- microbiology : Flax.
- pathogenicity : Basidiomycota.
- physiology : Basidiomycota.
- Biological Evolution, Genetic Variation, Genotype, Host-Parasite Interactions.
Abstract
Antagonistic coevolution is a critical force driving the evolution of diversity, yet the selective processes underpinning reciprocal adaptive changes in nature are not well understood. Local adaptation studies demonstrate partner impacts on fitness and adaptive change, but do not directly expose genetic processes predicted by theory. Specifically, we have little knowledge of the relative importance of fluctuating selection vs. arms-race dynamics in maintaining polymorphism in natural systems where metapopulation processes predominate. We conducted cross-year epidemiological, infection and genetic studies of multiple wild host and pathogen populations in the Linum-Melampsora association. We observed asynchronous phenotypic fluctuations in resistance and infectivity among demes. Importantly, changes in allelic frequencies at pathogen infectivity loci, and in host recognition of these genetic variants, correlated with disease prevalence during natural epidemics. These data strongly support reciprocal coevolution maintaining balanced resistance and infectivity polymorphisms, and highlight the importance of characterising spatial and temporal dynamics in antagonistic interactions.
DOI: 10.1111/j.1461-0248.2012.01749.x
PubMed: 22372578
PubMed Central: PMC3319837
Affiliations:
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Dodds</name></author><author><name sortKey="Barrett, Luke G" sort="Barrett, Luke G" uniqKey="Barrett L" first="Luke G" last="Barrett">Luke G. Barrett</name></author><author><name sortKey="Burdon, Jeremy J" sort="Burdon, Jeremy J" uniqKey="Burdon J" first="Jeremy J" last="Burdon">Jeremy J. Burdon</name></author></analytic><series><title level="j">Ecology letters</title><idno type="eISSN">1461-0248</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basidiomycota (genetics)</term><term>Basidiomycota (pathogenicity)</term><term>Basidiomycota (physiology)</term><term>Biological Evolution (MeSH)</term><term>Disease Resistance (genetics)</term><term>Flax (genetics)</term><term>Flax (microbiology)</term><term>Genetic Variation (MeSH)</term><term>Genotype (MeSH)</term><term>Host-Parasite Interactions (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Basidiomycota (génétique)</term><term>Basidiomycota (pathogénicité)</term><term>Basidiomycota (physiologie)</term><term>Génotype (MeSH)</term><term>Interactions hôte-parasite (MeSH)</term><term>Lin (génétique)</term><term>Lin (microbiologie)</term><term>Résistance à la maladie (génétique)</term><term>Variation génétique (MeSH)</term><term>Évolution biologique (MeSH)</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Basidiomycota</term><term>Disease Resistance</term><term>Flax</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Basidiomycota</term><term>Lin</term><term>Résistance à la maladie</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Lin</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Flax</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Basidiomycota</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Basidiomycota</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Basidiomycota</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Basidiomycota</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Biological Evolution</term><term>Genetic Variation</term><term>Genotype</term><term>Host-Parasite Interactions</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Génotype</term><term>Interactions hôte-parasite</term><term>Variation génétique</term><term>Évolution biologique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Antagonistic coevolution is a critical force driving the evolution of diversity, yet the selective processes underpinning reciprocal adaptive changes in nature are not well understood. Local adaptation studies demonstrate partner impacts on fitness and adaptive change, but do not directly expose genetic processes predicted by theory. Specifically, we have little knowledge of the relative importance of fluctuating selection vs. arms-race dynamics in maintaining polymorphism in natural systems where metapopulation processes predominate. We conducted cross-year epidemiological, infection and genetic studies of multiple wild host and pathogen populations in the Linum-Melampsora association. We observed asynchronous phenotypic fluctuations in resistance and infectivity among demes. Importantly, changes in allelic frequencies at pathogen infectivity loci, and in host recognition of these genetic variants, correlated with disease prevalence during natural epidemics. These data strongly support reciprocal coevolution maintaining balanced resistance and infectivity polymorphisms, and highlight the importance of characterising spatial and temporal dynamics in antagonistic interactions.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22372578</PMID><DateCompleted><Year>2012</Year><Month>06</Month><Day>14</Day></DateCompleted><DateRevised><Year>2019</Year><Month>01</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1461-0248</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>5</Issue><PubDate><Year>2012</Year><Month>May</Month></PubDate></JournalIssue><Title>Ecology letters</Title><ISOAbbreviation>Ecol Lett</ISOAbbreviation></Journal><ArticleTitle>Rapid genetic change underpins antagonistic coevolution in a natural host-pathogen metapopulation.</ArticleTitle><Pagination><MedlinePgn>425-35</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/j.1461-0248.2012.01749.x</ELocationID><Abstract><AbstractText>Antagonistic coevolution is a critical force driving the evolution of diversity, yet the selective processes underpinning reciprocal adaptive changes in nature are not well understood. Local adaptation studies demonstrate partner impacts on fitness and adaptive change, but do not directly expose genetic processes predicted by theory. Specifically, we have little knowledge of the relative importance of fluctuating selection vs. arms-race dynamics in maintaining polymorphism in natural systems where metapopulation processes predominate. We conducted cross-year epidemiological, infection and genetic studies of multiple wild host and pathogen populations in the Linum-Melampsora association. We observed asynchronous phenotypic fluctuations in resistance and infectivity among demes. Importantly, changes in allelic frequencies at pathogen infectivity loci, and in host recognition of these genetic variants, correlated with disease prevalence during natural epidemics. These data strongly support reciprocal coevolution maintaining balanced resistance and infectivity polymorphisms, and highlight the importance of characterising spatial and temporal dynamics in antagonistic interactions.</AbstractText><CopyrightInformation>© 2012 Blackwell Publishing Ltd/CNRS.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Thrall</LastName><ForeName>Peter H</ForeName><Initials>PH</Initials><AffiliationInfo><Affiliation>CSIRO Plant Industry, GPO Box 1600, Canberra, ACT 2601, Australia. peter.thrall@csiro.au</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laine</LastName><ForeName>Anna-Liisa</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Ravensdale</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Nemri</LastName><ForeName>Adnane</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Dodds</LastName><ForeName>Peter N</ForeName><Initials>PN</Initials></Author><Author ValidYN="Y"><LastName>Barrett</LastName><ForeName>Luke G</ForeName><Initials>LG</Initials></Author><Author ValidYN="Y"><LastName>Burdon</LastName><ForeName>Jeremy J</ForeName><Initials>JJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 GM074265</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 GM074265-01A2</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>5R01 GM074265-01A2</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016422">Letter</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>02</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Ecol Lett</MedlineTA><NlmUniqueID>101121949</NlmUniqueID><ISSNLinking>1461-023X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001487" MajorTopicYN="N">Basidiomycota</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005075" MajorTopicYN="Y">Biological Evolution</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D060467" MajorTopicYN="N">Disease Resistance</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019597" 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