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Plasmodium malariae and P. ovale genomes provide insights into malaria parasite evolution.

Identifieur interne : 000594 ( PubMed/Checkpoint ); précédent : 000593; suivant : 000595

Plasmodium malariae and P. ovale genomes provide insights into malaria parasite evolution.

Auteurs : Gavin G. Rutledge [Royaume-Uni] ; Ulrike Böhme [Royaume-Uni] ; Mandy Sanders [Royaume-Uni] ; Adam J. Reid [Royaume-Uni] ; James A. Cotton [Royaume-Uni] ; Oumou Maiga-Ascofare [Mali] ; Abdoulaye A. Djimdé [Royaume-Uni] ; Tobias O. Apinjoh ; Lucas Amenga-Etego [Ghana] ; Magnus Manske [Royaume-Uni] ; John W. Barnwell [États-Unis] ; François Renaud [France] ; Benjamin Ollomo [Gabon] ; Franck Prugnolle [France] ; Nicholas M. Anstey [Australie] ; Sarah Auburn [Australie] ; Ric N. Price [Australie] ; James S. Mccarthy [Australie] ; Dominic P. Kwiatkowski [Royaume-Uni] ; Chris I. Newbold [Royaume-Uni] ; Matthew Berriman [Royaume-Uni] ; Thomas D. Otto [Royaume-Uni]

Source :

RBID : pubmed:28117441

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English descriptors

Abstract

Elucidation of the evolutionary history and interrelatedness of Plasmodium species that infect humans has been hampered by a lack of genetic information for three human-infective species: P. malariae and two P. ovale species (P. o. curtisi and P. o. wallikeri). These species are prevalent across most regions in which malaria is endemic and are often undetectable by light microscopy, rendering their study in human populations difficult. The exact evolutionary relationship of these species to the other human-infective species has been contested. Using a new reference genome for P. malariae and a manually curated draft P. o. curtisi genome, we are now able to accurately place these species within the Plasmodium phylogeny. Sequencing of a P. malariae relative that infects chimpanzees reveals similar signatures of selection in the P. malariae lineage to another Plasmodium lineage shown to be capable of colonization of both human and chimpanzee hosts. Molecular dating suggests that these host adaptations occurred over similar evolutionary timescales. In addition to the core genome that is conserved between species, differences in gene content can be linked to their specific biology. The genome suggests that P. malariae expresses a family of heterodimeric proteins on its surface that have structural similarities to a protein crucial for invasion of red blood cells. The data presented here provide insight into the evolution of the Plasmodium genus as a whole.

DOI: 10.1038/nature21038
PubMed: 28117441


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pubmed:28117441

Le document en format XML

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<name sortKey="Auburn, Sarah" sort="Auburn, Sarah" uniqKey="Auburn S" first="Sarah" last="Auburn">Sarah Auburn</name>
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<title xml:lang="en">Plasmodium malariae and P. ovale genomes provide insights into malaria parasite evolution.</title>
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<name sortKey="Amenga Etego, Lucas" sort="Amenga Etego, Lucas" uniqKey="Amenga Etego L" first="Lucas" last="Amenga-Etego">Lucas Amenga-Etego</name>
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<name sortKey="Barnwell, John W" sort="Barnwell, John W" uniqKey="Barnwell J" first="John W" last="Barnwell">John W. Barnwell</name>
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<name sortKey="Renaud, Francois" sort="Renaud, Francois" uniqKey="Renaud F" first="François" last="Renaud">François Renaud</name>
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<name sortKey="Ollomo, Benjamin" sort="Ollomo, Benjamin" uniqKey="Ollomo B" first="Benjamin" last="Ollomo">Benjamin Ollomo</name>
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<name sortKey="Prugnolle, Franck" sort="Prugnolle, Franck" uniqKey="Prugnolle F" first="Franck" last="Prugnolle">Franck Prugnolle</name>
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<nlm:affiliation>Laboratoire MIVEGEC (UM1-CNRS-IRD), 34394 Montpellier, France.</nlm:affiliation>
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<title level="j">Nature</title>
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<term>Evolution, Molecular</term>
<term>Female</term>
<term>Genome (genetics)</term>
<term>Genomics</term>
<term>Humans</term>
<term>Malaria (parasitology)</term>
<term>Pan troglodytes (parasitology)</term>
<term>Phylogeny</term>
<term>Plasmodium malariae (genetics)</term>
<term>Plasmodium ovale (genetics)</term>
</keywords>
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<term>Animaux</term>
<term>Femelle</term>
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<term>Génomique</term>
<term>Humains</term>
<term>Paludisme (parasitologie)</term>
<term>Pan troglodytes (parasitologie)</term>
<term>Phylogénie</term>
<term>Plasmodium malariae (génétique)</term>
<term>Plasmodium ovale (génétique)</term>
<term>Érythrocytes (parasitologie)</term>
<term>Évolution moléculaire</term>
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<term>Genome</term>
<term>Plasmodium malariae</term>
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<term>Erythrocytes</term>
<term>Malaria</term>
<term>Pan troglodytes</term>
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<term>Animals</term>
<term>Evolution, Molecular</term>
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<front>
<div type="abstract" xml:lang="en">Elucidation of the evolutionary history and interrelatedness of Plasmodium species that infect humans has been hampered by a lack of genetic information for three human-infective species: P. malariae and two P. ovale species (P. o. curtisi and P. o. wallikeri). These species are prevalent across most regions in which malaria is endemic and are often undetectable by light microscopy, rendering their study in human populations difficult. The exact evolutionary relationship of these species to the other human-infective species has been contested. Using a new reference genome for P. malariae and a manually curated draft P. o. curtisi genome, we are now able to accurately place these species within the Plasmodium phylogeny. Sequencing of a P. malariae relative that infects chimpanzees reveals similar signatures of selection in the P. malariae lineage to another Plasmodium lineage shown to be capable of colonization of both human and chimpanzee hosts. Molecular dating suggests that these host adaptations occurred over similar evolutionary timescales. In addition to the core genome that is conserved between species, differences in gene content can be linked to their specific biology. The genome suggests that P. malariae expresses a family of heterodimeric proteins on its surface that have structural similarities to a protein crucial for invasion of red blood cells. The data presented here provide insight into the evolution of the Plasmodium genus as a whole.</div>
</front>
</TEI>
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<DateCreated>
<Year>2017</Year>
<Month>01</Month>
<Day>24</Day>
</DateCreated>
<DateCompleted>
<Year>2017</Year>
<Month>07</Month>
<Day>10</Day>
</DateCompleted>
<DateRevised>
<Year>2017</Year>
<Month>09</Month>
<Day>22</Day>
</DateRevised>
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<Journal>
<ISSN IssnType="Electronic">1476-4687</ISSN>
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<Volume>542</Volume>
<Issue>7639</Issue>
<PubDate>
<Year>2017</Year>
<Month>02</Month>
<Day>02</Day>
</PubDate>
</JournalIssue>
<Title>Nature</Title>
<ISOAbbreviation>Nature</ISOAbbreviation>
</Journal>
<ArticleTitle>Plasmodium malariae and P. ovale genomes provide insights into malaria parasite evolution.</ArticleTitle>
<Pagination>
<MedlinePgn>101-104</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/nature21038</ELocationID>
<Abstract>
<AbstractText>Elucidation of the evolutionary history and interrelatedness of Plasmodium species that infect humans has been hampered by a lack of genetic information for three human-infective species: P. malariae and two P. ovale species (P. o. curtisi and P. o. wallikeri). These species are prevalent across most regions in which malaria is endemic and are often undetectable by light microscopy, rendering their study in human populations difficult. The exact evolutionary relationship of these species to the other human-infective species has been contested. Using a new reference genome for P. malariae and a manually curated draft P. o. curtisi genome, we are now able to accurately place these species within the Plasmodium phylogeny. Sequencing of a P. malariae relative that infects chimpanzees reveals similar signatures of selection in the P. malariae lineage to another Plasmodium lineage shown to be capable of colonization of both human and chimpanzee hosts. Molecular dating suggests that these host adaptations occurred over similar evolutionary timescales. In addition to the core genome that is conserved between species, differences in gene content can be linked to their specific biology. The genome suggests that P. malariae expresses a family of heterodimeric proteins on its surface that have structural similarities to a protein crucial for invasion of red blood cells. The data presented here provide insight into the evolution of the Plasmodium genus as a whole.</AbstractText>
</Abstract>
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<ForeName>Gavin G</ForeName>
<Initials>GG</Initials>
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<Affiliation>Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.</Affiliation>
</AffiliationInfo>
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<LastName>Böhme</LastName>
<ForeName>Ulrike</ForeName>
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</AffiliationInfo>
</Author>
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<LastName>Sanders</LastName>
<ForeName>Mandy</ForeName>
<Initials>M</Initials>
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</AffiliationInfo>
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<ForeName>Adam J</ForeName>
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</AffiliationInfo>
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<LastName>Maiga-Ascofare</LastName>
<ForeName>Oumou</ForeName>
<Initials>O</Initials>
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<Affiliation>Malaria Research and Training Center, University of Science, Techniques, and Technologies of Bamako, Bamako BP E.2528, Mali.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>German Center for Infection Research, 20359 Hamburg, Germany.</Affiliation>
</AffiliationInfo>
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<ForeName>Abdoulaye A</ForeName>
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<Affiliation>Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Malaria Research and Training Center, University of Science, Techniques, and Technologies of Bamako, Bamako BP E.2528, Mali.</Affiliation>
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</AffiliationInfo>
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<Affiliation>Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.</Affiliation>
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<LastName>Price</LastName>
<ForeName>Ric N</ForeName>
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<AffiliationInfo>
<Affiliation>Global and Tropical Health Division, Menzies School of Health Research and Charles Darwin University, Darwin, Northern Territory 0810, Australia.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Centre for Tropical Medicine and Global Health, Nuffield Department of Clinical Medicine, University of Oxford, Oxford OX3 7LJ, UK.</Affiliation>
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<Author ValidYN="Y">
<LastName>McCarthy</LastName>
<ForeName>James S</ForeName>
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<Affiliation>Clinical Tropical Medicine Laboratory, QIMR Berghofer Medical Research Institute, University of Queensland, Brisbane, Queensland 4006, Australia.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y">
<LastName>Kwiatkowski</LastName>
<ForeName>Dominic P</ForeName>
<Initials>DP</Initials>
<AffiliationInfo>
<Affiliation>Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Newbold</LastName>
<ForeName>Chris I</ForeName>
<Initials>CI</Initials>
<AffiliationInfo>
<Affiliation>Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Berriman</LastName>
<ForeName>Matthew</ForeName>
<Initials>M</Initials>
<AffiliationInfo>
<Affiliation>Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Otto</LastName>
<ForeName>Thomas D</ForeName>
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