Phenotypic diversification is associated with host-induced transposon derepression in the sudden oak death pathogen Phytophthora ramorum.
Identifieur interne : 000227 ( Main/Exploration ); précédent : 000226; suivant : 000228Phenotypic diversification is associated with host-induced transposon derepression in the sudden oak death pathogen Phytophthora ramorum.
Auteurs : Takao Kasuga [États-Unis] ; Melina Kozanitas ; Mai Bui ; Daniel Hüberli ; David M. Rizzo ; Matteo GarbelottoSource :
- PloS one [ 1932-6203 ] ; 2012.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes (MeSH), Analyse de regroupements (MeSH), Arbres (MeSH), Californie (MeSH), Génotype (MeSH), Interactions hôte-pathogène (MeSH), Maladies des plantes (étiologie), Phytophthora (classification), Phytophthora (génétique), Phytophthora (pathogénicité), Phénotype (MeSH), Quercus (microbiologie), Reproductibilité des résultats (MeSH), Régulation de l'expression des gènes fongiques (MeSH), Répétitions microsatellites (MeSH), Rétroéléments (génétique), Umbellularia (microbiologie), Variation génétique (MeSH), Virulence (génétique).
- MESH :
- génétique : Phytophthora, Rétroéléments, Virulence.
- microbiologie : Quercus, Umbellularia.
- pathogénicité : Phytophthora.
- étiologie : Maladies des plantes.
- Analyse de profil d'expression de gènes, Analyse de regroupements, Arbres, Californie, Génotype, Interactions hôte-pathogène, Phénotype, Reproductibilité des résultats, Régulation de l'expression des gènes fongiques, Répétitions microsatellites, Variation génétique.
English descriptors
- KwdEn :
- California (MeSH), Cluster Analysis (MeSH), Gene Expression Profiling (MeSH), Gene Expression Regulation, Fungal (MeSH), Genetic Variation (MeSH), Genotype (MeSH), Host-Pathogen Interactions (MeSH), Microsatellite Repeats (MeSH), Phenotype (MeSH), Phytophthora (classification), Phytophthora (genetics), Phytophthora (pathogenicity), Plant Diseases (etiology), Quercus (microbiology), Reproducibility of Results (MeSH), Retroelements (genetics), Trees (MeSH), Umbellularia (microbiology), Virulence (genetics).
- MESH :
- chemical , genetics : Retroelements.
- geographic : California.
- classification : Phytophthora.
- etiology : Plant Diseases.
- genetics : Phytophthora, Virulence.
- microbiology : Quercus, Umbellularia.
- pathogenicity : Phytophthora.
- Cluster Analysis, Gene Expression Profiling, Gene Expression Regulation, Fungal, Genetic Variation, Genotype, Host-Pathogen Interactions, Microsatellite Repeats, Phenotype, Reproducibility of Results, Trees.
Abstract
The oomycete pathogen Phytophthora ramorum is responsible for sudden oak death (SOD) in California coastal forests. P. ramorum is a generalist pathogen with over 100 known host species. Three or four closely related genotypes of P. ramorum (from a single lineage) were originally introduced in California forests and the pathogen reproduces clonally. Because of this the genetic diversity of P. ramorum is extremely low in Californian forests. However, P. ramorum shows diverse phenotypic variation in colony morphology, colony senescence, and virulence. In this study, we show that phenotypic variation among isolates is associated with the host species from which the microbe was originally cultured. Microarray global mRNA profiling detected derepression of transposable elements (TEs) and down-regulation of crinkler effector homologs (CRNs) in the majority of isolates originating from coast live oak (Quercus agrifolia), but this expression pattern was not observed in isolates from California bay laurel (Umbellularia californica). In some instances, oak and bay laurel isolates originating from the same geographic location had identical genotypes based on multilocus simples sequence repeat (SSR) marker analysis but had different phenotypes. Expression levels of the two marker genes analyzed by quantitative reverse transcription PCR were correlated with originating host species, but not with multilocus genotypes. Because oak is a nontransmissive dead-end host for P. ramorum, our observations are congruent with an epi-transposon hypothesis; that is, physiological stress is triggered on P. ramorum while colonizing oak stems and disrupts epigenetic silencing of TEs. This then results in TE reactivation and possibly genome diversification without significant epidemiological consequences. We propose the P. ramorum-oak host system in California forests as an ad hoc model for epi-transposon mediated diversification.
DOI: 10.1371/journal.pone.0034728
PubMed: 22529930
PubMed Central: PMC3329494
Affiliations:
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P. ramorum is a generalist pathogen with over 100 known host species. Three or four closely related genotypes of P. ramorum (from a single lineage) were originally introduced in California forests and the pathogen reproduces clonally. Because of this the genetic diversity of P. ramorum is extremely low in Californian forests. However, P. ramorum shows diverse phenotypic variation in colony morphology, colony senescence, and virulence. In this study, we show that phenotypic variation among isolates is associated with the host species from which the microbe was originally cultured. Microarray global mRNA profiling detected derepression of transposable elements (TEs) and down-regulation of crinkler effector homologs (CRNs) in the majority of isolates originating from coast live oak (Quercus agrifolia), but this expression pattern was not observed in isolates from California bay laurel (Umbellularia californica). In some instances, oak and bay laurel isolates originating from the same geographic location had identical genotypes based on multilocus simples sequence repeat (SSR) marker analysis but had different phenotypes. Expression levels of the two marker genes analyzed by quantitative reverse transcription PCR were correlated with originating host species, but not with multilocus genotypes. Because oak is a nontransmissive dead-end host for P. ramorum, our observations are congruent with an epi-transposon hypothesis; that is, physiological stress is triggered on P. ramorum while colonizing oak stems and disrupts epigenetic silencing of TEs. This then results in TE reactivation and possibly genome diversification without significant epidemiological consequences. We propose the P. ramorum-oak host system in California forests as an ad hoc model for epi-transposon mediated diversification.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22529930</PMID><DateCompleted><Year>2012</Year><Month>11</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>4</Issue><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Phenotypic diversification is associated with host-induced transposon derepression in the sudden oak death pathogen Phytophthora ramorum.</ArticleTitle><Pagination><MedlinePgn>e34728</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0034728</ELocationID><Abstract><AbstractText>The oomycete pathogen Phytophthora ramorum is responsible for sudden oak death (SOD) in California coastal forests. P. ramorum is a generalist pathogen with over 100 known host species. Three or four closely related genotypes of P. ramorum (from a single lineage) were originally introduced in California forests and the pathogen reproduces clonally. Because of this the genetic diversity of P. ramorum is extremely low in Californian forests. However, P. ramorum shows diverse phenotypic variation in colony morphology, colony senescence, and virulence. In this study, we show that phenotypic variation among isolates is associated with the host species from which the microbe was originally cultured. Microarray global mRNA profiling detected derepression of transposable elements (TEs) and down-regulation of crinkler effector homologs (CRNs) in the majority of isolates originating from coast live oak (Quercus agrifolia), but this expression pattern was not observed in isolates from California bay laurel (Umbellularia californica). In some instances, oak and bay laurel isolates originating from the same geographic location had identical genotypes based on multilocus simples sequence repeat (SSR) marker analysis but had different phenotypes. Expression levels of the two marker genes analyzed by quantitative reverse transcription PCR were correlated with originating host species, but not with multilocus genotypes. Because oak is a nontransmissive dead-end host for P. ramorum, our observations are congruent with an epi-transposon hypothesis; that is, physiological stress is triggered on P. ramorum while colonizing oak stems and disrupts epigenetic silencing of TEs. This then results in TE reactivation and possibly genome diversification without significant epidemiological consequences. We propose the P. ramorum-oak host system in California forests as an ad hoc model for epi-transposon mediated diversification.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kasuga</LastName><ForeName>Takao</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Crops Pathology and Genetics Research Unit, United States Department of Agriculture-Agricultural Research Service, Davis, California, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kozanitas</LastName><ForeName>Melina</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Bui</LastName><ForeName>Mai</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Hüberli</LastName><ForeName>Daniel</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Rizzo</LastName><ForeName>David M</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Garbelotto</LastName><ForeName>Matteo</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>EF-0622770</GrantID><Agency>PHS HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>04</Month><Day>18</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 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Repeats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="Y">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010838" MajorTopicYN="N">Phytophthora</DescriptorName><QualifierName UI="Q000145" MajorTopicYN="N">classification</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029963" MajorTopicYN="N">Quercus</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015203" MajorTopicYN="N">Reproducibility of Results</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018626" MajorTopicYN="N">Retroelements</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014197" MajorTopicYN="N">Trees</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D027422" MajorTopicYN="N">Umbellularia</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>01</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>03</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>4</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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sort="Garbelotto, Matteo" uniqKey="Garbelotto M" first="Matteo" last="Garbelotto">Matteo Garbelotto</name><name sortKey="Huberli, Daniel" sort="Huberli, Daniel" uniqKey="Huberli D" first="Daniel" last="Hüberli">Daniel Hüberli</name><name sortKey="Kozanitas, Melina" sort="Kozanitas, Melina" uniqKey="Kozanitas M" first="Melina" last="Kozanitas">Melina Kozanitas</name><name sortKey="Rizzo, David M" sort="Rizzo, David M" uniqKey="Rizzo D" first="David M" last="Rizzo">David M. Rizzo</name></noCountry><country name="États-Unis"><region name="Californie"><name sortKey="Kasuga, Takao" sort="Kasuga, Takao" uniqKey="Kasuga T" first="Takao" last="Kasuga">Takao Kasuga</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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