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Article: Rapid evolution of disease resistance is accompanied by functional changes in gene expression in a wild bird

TitleRapid evolution of disease resistance is accompanied by functional changes in gene expression in a wild bird
Authors
Issue Date2011
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 2011, v. 108 n. 19, p. 7866-7871 How to Cite?
AbstractWild organisms are under increasing pressure to adapt rapidly to environmental changes. Predicting the impact of these changes on natural populations requires an understanding of the speed with which adaptive phenotypes can arise and spread, as well as of the underlying mechanisms. However, our understanding of these parameters is poor in natural populations. Here we use experimental and molecular approaches to investigate the recent emergence of resistance in eastern populations of North American house finches (Carpodacus mexicanus) to Mycoplasma galliseptum (MG), a severe conjunctivitis-causing bacterium. Two weeks following an experimental infection that took place in 2007, finches from eastern US populations with a 12-y history of exposure to MG harbored 33% lower MG loads in their conjunctivae than finches from western US populations with no prior exposure to MG. Using a cDNA microarray, we show that this phenotypic difference in resistance was associated with differences in splenic gene expression, with finches from the exposed populations up-regulating immune genes postinfection and those from the unexposed populations generally down-regulating them. The expression response of western US birds to experimental infection in 2007 was more similar to that of the eastern US birds studied in 2000, 7 y earlier in the epizootic, than to that of eastern birds in 2007. These results support the hypothesis that resistance has evolved by natural selection in the exposed populations over the 12 y of the epizootic.Wehypothesize that host resistance arose and spread from standing genetic variation in the eastern US and highlight that natural selection can lead to rapid phenotypic evolution in populations when acting on such variation.
Persistent Identifierhttp://hdl.handle.net/10722/180747
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBonneaud, Cen_US
dc.contributor.authorBalenger, SLen_US
dc.contributor.authorRussell, AFen_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorHill, GEen_US
dc.contributor.authorEdwards, SVen_US
dc.date.accessioned2013-01-28T01:42:13Z-
dc.date.available2013-01-28T01:42:13Z-
dc.date.issued2011en_US
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2011, v. 108 n. 19, p. 7866-7871en_US
dc.identifier.issn0027-8424en_US
dc.identifier.urihttp://hdl.handle.net/10722/180747-
dc.description.abstractWild organisms are under increasing pressure to adapt rapidly to environmental changes. Predicting the impact of these changes on natural populations requires an understanding of the speed with which adaptive phenotypes can arise and spread, as well as of the underlying mechanisms. However, our understanding of these parameters is poor in natural populations. Here we use experimental and molecular approaches to investigate the recent emergence of resistance in eastern populations of North American house finches (Carpodacus mexicanus) to Mycoplasma galliseptum (MG), a severe conjunctivitis-causing bacterium. Two weeks following an experimental infection that took place in 2007, finches from eastern US populations with a 12-y history of exposure to MG harbored 33% lower MG loads in their conjunctivae than finches from western US populations with no prior exposure to MG. Using a cDNA microarray, we show that this phenotypic difference in resistance was associated with differences in splenic gene expression, with finches from the exposed populations up-regulating immune genes postinfection and those from the unexposed populations generally down-regulating them. The expression response of western US birds to experimental infection in 2007 was more similar to that of the eastern US birds studied in 2000, 7 y earlier in the epizootic, than to that of eastern birds in 2007. These results support the hypothesis that resistance has evolved by natural selection in the exposed populations over the 12 y of the epizootic.Wehypothesize that host resistance arose and spread from standing genetic variation in the eastern US and highlight that natural selection can lead to rapid phenotypic evolution in populations when acting on such variation.en_US
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_US
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_US
dc.subject.meshAlabamaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArizonaen_US
dc.subject.meshBiological Evolutionen_US
dc.subject.meshBird Diseases - Genetics - Immunology - Microbiologyen_US
dc.subject.meshBirds - Genetics - Immunology - Microbiologyen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshMaleen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMycobacterium - Immunology - Pathogenicityen_US
dc.subject.meshMycobacterium Infections - Genetics - Immunology - Microbiology - Veterinaryen_US
dc.subject.meshOligonucleotide Array Sequence Analysisen_US
dc.subject.meshSpleen - Immunology - Metabolismen_US
dc.titleRapid evolution of disease resistance is accompanied by functional changes in gene expression in a wild birden_US
dc.typeArticleen_US
dc.identifier.emailZhang, J: jzhang1@hku.hken_US
dc.identifier.authorityZhang, J=rp01713en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1073/pnas.1018580108en_US
dc.identifier.pmid21525409-
dc.identifier.scopuseid_2-s2.0-79956339215en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79956339215&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume108en_US
dc.identifier.issue19en_US
dc.identifier.spage7866en_US
dc.identifier.epage7871en_US
dc.identifier.isiWOS:000290439500082-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBonneaud, C=6507932232en_US
dc.identifier.scopusauthoridBalenger, SL=6506097429en_US
dc.identifier.scopusauthoridRussell, AF=7402736301en_US
dc.identifier.scopusauthoridZhang, J=22137260600en_US
dc.identifier.scopusauthoridHill, GE=35500077500en_US
dc.identifier.scopusauthoridEdwards, SV=7401520541en_US

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