Genome analyses of the wheat yellow (stripe) rust pathogen Puccinia striiformis f. sp. tritici reveal polymorphic and haustorial expressed secreted proteins as candidate effectors.
Identifieur interne : 000114 ( Main/Exploration ); précédent : 000113; suivant : 000115Genome analyses of the wheat yellow (stripe) rust pathogen Puccinia striiformis f. sp. tritici reveal polymorphic and haustorial expressed secreted proteins as candidate effectors.
Auteurs : Dario Cantu [États-Unis] ; Vanesa Segovia ; Daniel Maclean ; Rosemary Bayles ; Xianming Chen ; Sophien Kamoun ; Jorge Dubcovsky ; Diane G O. Saunders ; Cristobal UauySource :
- BMC genomics [ 1471-2164 ] ; 2013.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Basidiomycota, Maladies des plantes, Protéines fongiques.
- microbiologie : Triticum.
- métabolisme : Protéines fongiques.
- pathogénicité : Basidiomycota.
- Génome fongique, Polymorphisme génétique, Virulence.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Fungal Proteins.
- genetics : Basidiomycota, Plant Diseases.
- chemical , metabolism : Fungal Proteins.
- microbiology : Triticum.
- pathogenicity : Basidiomycota.
- Genome, Fungal, Polymorphism, Genetic, Virulence.
Abstract
BACKGROUND
Wheat yellow (stripe) rust caused by Puccinia striiformis f. sp. tritici (PST) is one of the most devastating diseases of wheat worldwide. To design effective breeding strategies that maximize the potential for durable disease resistance it is important to understand the molecular basis of PST pathogenicity. In particular, the characterisation of the structure, function and evolutionary dynamics of secreted effector proteins that are detected by host immune receptors can help guide and prioritize breeding efforts. However, to date, our knowledge of the effector repertoire of cereal rust pathogens is limited.
RESULTS
We re-sequenced genomes of four PST isolates from the US and UK to identify effector candidates and relate them to their distinct virulence profiles. First, we assessed SNP frequencies between all isolates, with heterokaryotic SNPs being over tenfold more frequent (5.29 ± 2.23 SNPs/kb) than homokaryotic SNPs (0.41 ± 0.28 SNPs/kb). Next, we implemented a bioinformatics pipeline to integrate genomics, transcriptomics, and effector-focused annotations to identify and classify effector candidates in PST. RNAseq analysis highlighted transcripts encoding secreted proteins that were significantly enriched in haustoria compared to infected tissue. The expression of 22 candidate effector genes was characterised using qRT-PCR, revealing distinct temporal expression patterns during infection in wheat. Lastly, we identified proteins that displayed non-synonymous substitutions specifically between the two UK isolates PST-87/7 and PST-08/21, which differ in virulence to two wheat varieties. By focusing on polymorphic variants enriched in haustoria, we identified five polymorphic effector candidates between PST-87/7 and PST-08/21 among 2,999 secreted proteins. These allelic variants are now a priority for functional validation as virulence/avirulence effectors in the corresponding wheat varieties.
CONCLUSIONS
Integration of genomics, transcriptomics, and effector-directed annotation of PST isolates has enabled us to move beyond the single isolate-directed catalogues of effector proteins and develop a framework for mining effector proteins in closely related isolates and relate these back to their defined virulence profiles. This should ultimately lead to more comprehensive understanding of the PST pathogenesis system, an important first step towards developing more effective surveillance and management strategies for one of the most devastating pathogens of wheat.
DOI: 10.1186/1471-2164-14-270
PubMed: 23607900
PubMed Central: PMC3640902
Affiliations:
Links toward previous steps (curation, corpus...)
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Saunders</name></author><author><name sortKey="Uauy, Cristobal" sort="Uauy, Cristobal" uniqKey="Uauy C" first="Cristobal" last="Uauy">Cristobal Uauy</name></author></analytic><series><title level="j">BMC genomics</title><idno type="eISSN">1471-2164</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basidiomycota (genetics)</term><term>Basidiomycota (pathogenicity)</term><term>Fungal Proteins (genetics)</term><term>Fungal Proteins (metabolism)</term><term>Genome, Fungal (MeSH)</term><term>Plant Diseases (genetics)</term><term>Polymorphism, Genetic (MeSH)</term><term>Triticum (microbiology)</term><term>Virulence (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Basidiomycota (génétique)</term><term>Basidiomycota (pathogénicité)</term><term>Génome fongique (MeSH)</term><term>Maladies des plantes (génétique)</term><term>Polymorphisme génétique (MeSH)</term><term>Protéines fongiques (génétique)</term><term>Protéines fongiques (métabolisme)</term><term>Triticum (microbiologie)</term><term>Virulence (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fungal Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Basidiomycota</term><term>Plant Diseases</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Basidiomycota</term><term>Maladies des plantes</term><term>Protéines fongiques</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fungal Proteins</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Triticum</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Triticum</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines fongiques</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" xml:lang="en"><term>Genome, Fungal</term><term>Polymorphism, Genetic</term><term>Virulence</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Génome fongique</term><term>Polymorphisme génétique</term><term>Virulence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b></p><p>Wheat yellow (stripe) rust caused by Puccinia striiformis f. sp. tritici (PST) is one of the most devastating diseases of wheat worldwide. To design effective breeding strategies that maximize the potential for durable disease resistance it is important to understand the molecular basis of PST pathogenicity. In particular, the characterisation of the structure, function and evolutionary dynamics of secreted effector proteins that are detected by host immune receptors can help guide and prioritize breeding efforts. However, to date, our knowledge of the effector repertoire of cereal rust pathogens is limited.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>We re-sequenced genomes of four PST isolates from the US and UK to identify effector candidates and relate them to their distinct virulence profiles. First, we assessed SNP frequencies between all isolates, with heterokaryotic SNPs being over tenfold more frequent (5.29 ± 2.23 SNPs/kb) than homokaryotic SNPs (0.41 ± 0.28 SNPs/kb). Next, we implemented a bioinformatics pipeline to integrate genomics, transcriptomics, and effector-focused annotations to identify and classify effector candidates in PST. RNAseq analysis highlighted transcripts encoding secreted proteins that were significantly enriched in haustoria compared to infected tissue. The expression of 22 candidate effector genes was characterised using qRT-PCR, revealing distinct temporal expression patterns during infection in wheat. Lastly, we identified proteins that displayed non-synonymous substitutions specifically between the two UK isolates PST-87/7 and PST-08/21, which differ in virulence to two wheat varieties. By focusing on polymorphic variants enriched in haustoria, we identified five polymorphic effector candidates between PST-87/7 and PST-08/21 among 2,999 secreted proteins. These allelic variants are now a priority for functional validation as virulence/avirulence effectors in the corresponding wheat varieties.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Integration of genomics, transcriptomics, and effector-directed annotation of PST isolates has enabled us to move beyond the single isolate-directed catalogues of effector proteins and develop a framework for mining effector proteins in closely related isolates and relate these back to their defined virulence profiles. This should ultimately lead to more comprehensive understanding of the PST pathogenesis system, an important first step towards developing more effective surveillance and management strategies for one of the most devastating pathogens of wheat.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23607900</PMID><DateCompleted><Year>2013</Year><Month>10</Month><Day>24</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-2164</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><PubDate><Year>2013</Year><Month>Apr</Month><Day>22</Day></PubDate></JournalIssue><Title>BMC genomics</Title><ISOAbbreviation>BMC Genomics</ISOAbbreviation></Journal><ArticleTitle>Genome analyses of the wheat yellow (stripe) rust pathogen Puccinia striiformis f. sp. tritici reveal polymorphic and haustorial expressed secreted proteins as candidate effectors.</ArticleTitle><Pagination><MedlinePgn>270</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/1471-2164-14-270</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Wheat yellow (stripe) rust caused by Puccinia striiformis f. sp. tritici (PST) is one of the most devastating diseases of wheat worldwide. To design effective breeding strategies that maximize the potential for durable disease resistance it is important to understand the molecular basis of PST pathogenicity. In particular, the characterisation of the structure, function and evolutionary dynamics of secreted effector proteins that are detected by host immune receptors can help guide and prioritize breeding efforts. However, to date, our knowledge of the effector repertoire of cereal rust pathogens is limited.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We re-sequenced genomes of four PST isolates from the US and UK to identify effector candidates and relate them to their distinct virulence profiles. First, we assessed SNP frequencies between all isolates, with heterokaryotic SNPs being over tenfold more frequent (5.29 ± 2.23 SNPs/kb) than homokaryotic SNPs (0.41 ± 0.28 SNPs/kb). Next, we implemented a bioinformatics pipeline to integrate genomics, transcriptomics, and effector-focused annotations to identify and classify effector candidates in PST. RNAseq analysis highlighted transcripts encoding secreted proteins that were significantly enriched in haustoria compared to infected tissue. The expression of 22 candidate effector genes was characterised using qRT-PCR, revealing distinct temporal expression patterns during infection in wheat. Lastly, we identified proteins that displayed non-synonymous substitutions specifically between the two UK isolates PST-87/7 and PST-08/21, which differ in virulence to two wheat varieties. By focusing on polymorphic variants enriched in haustoria, we identified five polymorphic effector candidates between PST-87/7 and PST-08/21 among 2,999 secreted proteins. These allelic variants are now a priority for functional validation as virulence/avirulence effectors in the corresponding wheat varieties.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Integration of genomics, transcriptomics, and effector-directed annotation of PST isolates has enabled us to move beyond the single isolate-directed catalogues of effector proteins and develop a framework for mining effector proteins in closely related isolates and relate these back to their defined virulence profiles. This should ultimately lead to more comprehensive understanding of the PST pathogenesis system, an important first step towards developing more effective surveillance and management strategies for one of the most devastating pathogens of wheat.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cantu</LastName><ForeName>Dario</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Viticulture & Enology, University of California Davis, Davis, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Segovia</LastName><ForeName>Vanesa</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>MacLean</LastName><ForeName>Daniel</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Bayles</LastName><ForeName>Rosemary</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xianming</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Kamoun</LastName><ForeName>Sophien</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Dubcovsky</LastName><ForeName>Jorge</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Saunders</LastName><ForeName>Diane G O</ForeName><Initials>DG</Initials></Author><Author ValidYN="Y"><LastName>Uauy</LastName><ForeName>Cristobal</ForeName><Initials>C</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>BB/J004553/1</GrantID><Agency>Biotechnology and Biological Sciences Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>BB/J004596/1</GrantID><Agency>Biotechnology and Biological Sciences Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>BB/J012017/1</GrantID><Agency>Biotechnology and Biological Sciences Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Howard Hughes Medical Institute</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</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>2013</Year><Month>04</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Genomics</MedlineTA><NlmUniqueID>100965258</NlmUniqueID><ISSNLinking>1471-2164</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001487" MajorTopicYN="N">Basidiomycota</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005656" MajorTopicYN="N">Fungal Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016681" MajorTopicYN="Y">Genome, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011110" MajorTopicYN="N">Polymorphism, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014908" MajorTopicYN="N">Triticum</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014774" 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last="Kamoun">Sophien Kamoun</name><name sortKey="Maclean, Daniel" sort="Maclean, Daniel" uniqKey="Maclean D" first="Daniel" last="Maclean">Daniel Maclean</name><name sortKey="Saunders, Diane G O" sort="Saunders, Diane G O" uniqKey="Saunders D" first="Diane G O" last="Saunders">Diane G O. Saunders</name><name sortKey="Segovia, Vanesa" sort="Segovia, Vanesa" uniqKey="Segovia V" first="Vanesa" last="Segovia">Vanesa Segovia</name><name sortKey="Uauy, Cristobal" sort="Uauy, Cristobal" uniqKey="Uauy C" first="Cristobal" last="Uauy">Cristobal Uauy</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Cantu, Dario" sort="Cantu, Dario" uniqKey="Cantu D" first="Dario" last="Cantu">Dario Cantu</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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