Functional Profiling of a Plasmodium Genome Reveals an Abundance of Essential Genes
Identifieur interne : 002225 ( Pmc/Curation ); précédent : 002224; suivant : 002226Functional Profiling of a Plasmodium Genome Reveals an Abundance of Essential Genes
Auteurs : Ellen Bushell [Royaume-Uni] ; Ana Rita Gomes [Royaume-Uni] ; Theo Sanderson [Royaume-Uni] ; Burcu Anar [Royaume-Uni] ; Gareth Girling [Royaume-Uni] ; Colin Herd [Royaume-Uni] ; Tom Metcalf [Royaume-Uni] ; Katarzyna Modrzynska [Royaume-Uni] ; Frank Schwach [Royaume-Uni] ; Rowena E. Martin [Australie] ; Michael W. Mather [États-Unis] ; Geoffrey I. Mcfadden [Australie] ; Leopold Parts [Royaume-Uni] ; Gavin G. Rutledge [Royaume-Uni] ; Akhil B. Vaidya [États-Unis] ; Kai Wengelnik [France] ; Julian C. Rayner [Royaume-Uni] ; Oliver Billker [Royaume-Uni]Source :
- Cell [ 0092-8674 ] ; 2017.
Abstract
The genomes of malaria parasites contain many genes of unknown function. To assist drug development through the identification of essential genes and pathways, we have measured competitive growth rates in mice of 2,578 barcoded
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DOI: 10.1016/j.cell.2017.06.030
PubMed: 28708996
PubMed Central: 5509546
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xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Gomes, Ana Rita" sort="Gomes, Ana Rita" uniqKey="Gomes A" first="Ana Rita" last="Gomes">Ana Rita Gomes</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Sanderson, Theo" sort="Sanderson, Theo" uniqKey="Sanderson T" first="Theo" last="Sanderson">Theo Sanderson</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger 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Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Herd, Colin" sort="Herd, Colin" uniqKey="Herd C" first="Colin" last="Herd">Colin Herd</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Metcalf, Tom" sort="Metcalf, Tom" uniqKey="Metcalf T" first="Tom" last="Metcalf">Tom Metcalf</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Modrzynska, Katarzyna" sort="Modrzynska, Katarzyna" uniqKey="Modrzynska K" first="Katarzyna" last="Modrzynska">Katarzyna Modrzynska</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Schwach, Frank" sort="Schwach, Frank" uniqKey="Schwach F" first="Frank" last="Schwach">Frank Schwach</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Martin, Rowena E" sort="Martin, Rowena E" uniqKey="Martin R" first="Rowena E." last="Martin">Rowena E. Martin</name><affiliation wicri:level="1"><nlm:aff id="aff2">Research School of Biology, Australian National University, Canberra, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Research School of Biology, Australian National University, Canberra</wicri:regionArea></affiliation></author><author><name sortKey="Mather, Michael W" sort="Mather, Michael W" uniqKey="Mather M" first="Michael W." last="Mather">Michael W. Mather</name><affiliation wicri:level="1"><nlm:aff id="aff3">Drexel University College of Medicine, Philadelphia, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Drexel University College of Medicine, Philadelphia, PA</wicri:regionArea></affiliation></author><author><name sortKey="Mcfadden, Geoffrey I" sort="Mcfadden, Geoffrey I" uniqKey="Mcfadden G" first="Geoffrey I." last="Mcfadden">Geoffrey I. Mcfadden</name><affiliation wicri:level="1"><nlm:aff id="aff4">School of Biosciences, University of Melbourne, Royal Parade, Parkville, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>School of Biosciences, University of Melbourne, Royal Parade, Parkville</wicri:regionArea></affiliation></author><author><name sortKey="Parts, Leopold" sort="Parts, Leopold" uniqKey="Parts L" first="Leopold" last="Parts">Leopold Parts</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Rutledge, Gavin G" sort="Rutledge, Gavin G" uniqKey="Rutledge G" first="Gavin G." last="Rutledge">Gavin G. Rutledge</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Vaidya, Akhil B" sort="Vaidya, Akhil B" uniqKey="Vaidya A" first="Akhil B." last="Vaidya">Akhil B. Vaidya</name><affiliation wicri:level="1"><nlm:aff id="aff3">Drexel University College of Medicine, Philadelphia, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Drexel University College of Medicine, Philadelphia, PA</wicri:regionArea></affiliation></author><author><name sortKey="Wengelnik, Kai" sort="Wengelnik, Kai" uniqKey="Wengelnik K" first="Kai" last="Wengelnik">Kai Wengelnik</name><affiliation wicri:level="1"><nlm:aff id="aff5">DIMNP, CNRS, INSERM, University Montpellier, Montpellier, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>DIMNP, CNRS, INSERM, University Montpellier, Montpellier</wicri:regionArea></affiliation></author><author><name sortKey="Rayner, Julian C" sort="Rayner, Julian C" uniqKey="Rayner J" first="Julian C." last="Rayner">Julian C. Rayner</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author><author><name sortKey="Billker, Oliver" sort="Billker, Oliver" uniqKey="Billker O" first="Oliver" last="Billker">Oliver Billker</name><affiliation wicri:level="1"><nlm:aff id="aff1">Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cell</title><idno type="ISSN">0092-8674</idno><idno type="eISSN">1097-4172</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Summary</title><p>The genomes of malaria parasites contain many genes of unknown function. To assist drug development through the identification of essential genes and pathways, we have measured competitive growth rates in mice of 2,578 barcoded <italic>Plasmodium berghei</italic> knockout mutants, representing >50% of the genome, and created a phenotype database. At a single stage of its complex life cycle, <italic>P. berghei</italic> requires two-thirds of genes for optimal growth, the highest proportion reported from any organism and a probable consequence of functional optimization necessitated by genomic reductions during the evolution of parasitism. In contrast, extreme functional redundancy has evolved among expanded gene families operating at the parasite-host interface. The level of genetic redundancy in a single-celled organism may thus reflect the degree of environmental variation it experiences. In the case of <italic>Plasmodium</italic> parasites, this helps rationalize both the relative successes of drugs and the greater difficulty of making an effective vaccine.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Alexa, A" uniqKey="Alexa A">A. Alexa</name></author><author><name sortKey="Rahnenfuhrer, J" uniqKey="Rahnenfuhrer J">J. Rahnenführer</name></author><author><name sortKey="Lengauer, T" uniqKey="Lengauer T">T. Lengauer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Alsford, S" uniqKey="Alsford S">S. Alsford</name></author><author><name sortKey="Turner, D J" uniqKey="Turner D">D.J. Turner</name></author><author><name sortKey="Obado, S O" uniqKey="Obado S">S.O. Obado</name></author><author><name sortKey="Sanchez Flores, A" uniqKey="Sanchez Flores A">A. Sanchez-Flores</name></author><author><name sortKey="Glover, L" uniqKey="Glover L">L. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell</journal-id><journal-id journal-id-type="iso-abbrev">Cell</journal-id><journal-title-group><journal-title>Cell</journal-title></journal-title-group><issn pub-type="ppub">0092-8674</issn><issn pub-type="epub">1097-4172</issn><publisher><publisher-name>Cell Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">28708996</article-id><article-id pub-id-type="pmc">5509546</article-id><article-id pub-id-type="publisher-id">S0092-8674(17)30714-6</article-id><article-id pub-id-type="doi">10.1016/j.cell.2017.06.030</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Functional Profiling of a <italic>Plasmodium</italic> Genome Reveals an Abundance of Essential Genes</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Bushell</surname><given-names>Ellen</given-names></name><xref rid="aff1" ref-type="aff">1</xref><xref rid="fn1" ref-type="fn">6</xref></contrib><contrib contrib-type="author"><name><surname>Gomes</surname><given-names>Ana Rita</given-names></name><xref rid="aff1" ref-type="aff">1</xref><xref rid="fn1" ref-type="fn">6</xref></contrib><contrib contrib-type="author"><name><surname>Sanderson</surname><given-names>Theo</given-names></name><xref rid="aff1" ref-type="aff">1</xref><xref rid="fn1" ref-type="fn">6</xref></contrib><contrib contrib-type="author"><name><surname>Anar</surname><given-names>Burcu</given-names></name><xref rid="aff1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Girling</surname><given-names>Gareth</given-names></name><xref rid="aff1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Herd</surname><given-names>Colin</given-names></name><xref rid="aff1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Metcalf</surname><given-names>Tom</given-names></name><xref rid="aff1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Modrzynska</surname><given-names>Katarzyna</given-names></name><xref rid="aff1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Schwach</surname><given-names>Frank</given-names></name><xref rid="aff1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Martin</surname><given-names>Rowena E.</given-names></name><xref rid="aff2" ref-type="aff">2</xref></contrib><contrib contrib-type="author"><name><surname>Mather</surname><given-names>Michael W.</given-names></name><xref rid="aff3" ref-type="aff">3</xref></contrib><contrib contrib-type="author"><name><surname>McFadden</surname><given-names>Geoffrey I.</given-names></name><xref rid="aff4" ref-type="aff">4</xref></contrib><contrib contrib-type="author"><name><surname>Parts</surname><given-names>Leopold</given-names></name><xref rid="aff1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Rutledge</surname><given-names>Gavin G.</given-names></name><xref rid="aff1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Vaidya</surname><given-names>Akhil B.</given-names></name><xref rid="aff3" ref-type="aff">3</xref></contrib><contrib contrib-type="author"><name><surname>Wengelnik</surname><given-names>Kai</given-names></name><xref rid="aff5" ref-type="aff">5</xref></contrib><contrib contrib-type="author"><name><surname>Rayner</surname><given-names>Julian C.</given-names></name><email>julian.rayner@sanger.ac.uk</email><xref rid="aff1" ref-type="aff">1</xref><xref rid="cor1" ref-type="corresp">∗</xref></contrib><contrib contrib-type="author"><name><surname>Billker</surname><given-names>Oliver</given-names></name><email>oliver.billker@sanger.ac.uk</email><xref rid="aff1" ref-type="aff">1</xref><xref rid="fn2" ref-type="fn">7</xref><xref rid="cor2" ref-type="corresp">∗∗</xref></contrib></contrib-group><aff id="aff1"><label>1</label>Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK</aff><aff id="aff2"><label>2</label>Research School of Biology, Australian National University, Canberra, Australia</aff><aff id="aff3"><label>3</label>Drexel University College of Medicine, Philadelphia, PA, USA</aff><aff id="aff4"><label>4</label>School of Biosciences, University of Melbourne, Royal Parade, Parkville, Australia</aff><aff id="aff5"><label>5</label>DIMNP, CNRS, INSERM, University Montpellier, Montpellier, France</aff><author-notes><corresp id="cor1"><label>∗</label>Corresponding author <email>julian.rayner@sanger.ac.uk</email></corresp><corresp id="cor2"><label>∗∗</label>Corresponding author <email>oliver.billker@sanger.ac.uk</email></corresp><fn id="fn1"><label>6</label><p id="ntpara0010">These authors contributed equally</p></fn><fn id="fn2"><label>7</label><p id="ntpara0015">Lead Contact</p></fn></author-notes><pub-date pub-type="pmc-release"><day>13</day><month>7</month><year>2017</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><day>13</day><month>7</month><year>2017</year></pub-date><volume>170</volume><issue>2</issue><fpage>260</fpage><lpage>272.e8</lpage><history><date date-type="received"><day>16</day><month>11</month><year>2016</year></date><date date-type="rev-recd"><day>13</day><month>4</month><year>2017</year></date><date date-type="accepted"><day>19</day><month>6</month><year>2017</year></date></history><permissions><copyright-statement>© 2017 The Authors</copyright-statement><copyright-year>2017</copyright-year><license license-type="CC BY" xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).</license-p></license></permissions><abstract id="abs0010"><title>Summary</title><p>The genomes of malaria parasites contain many genes of unknown function. To assist drug development through the identification of essential genes and pathways, we have measured competitive growth rates in mice of 2,578 barcoded <italic>Plasmodium berghei</italic> knockout mutants, representing >50% of the genome, and created a phenotype database. At a single stage of its complex life cycle, <italic>P. berghei</italic> requires two-thirds of genes for optimal growth, the highest proportion reported from any organism and a probable consequence of functional optimization necessitated by genomic reductions during the evolution of parasitism. In contrast, extreme functional redundancy has evolved among expanded gene families operating at the parasite-host interface. The level of genetic redundancy in a single-celled organism may thus reflect the degree of environmental variation it experiences. In the case of <italic>Plasmodium</italic> parasites, this helps rationalize both the relative successes of drugs and the greater difficulty of making an effective vaccine.</p></abstract><abstract abstract-type="graphical" id="abs0015"><title>Graphical Abstract</title><fig id="undfig1" position="anchor"><graphic xlink:href="fx1"></graphic></fig></abstract><abstract abstract-type="author-highlights" id="abs0020"><title>Highlights</title><p><list list-type="simple"><list-item id="u0010"><label>•</label><p>Two-thirds of <italic>Plasmodium berghei</italic> genes contribute to normal blood stage growth</p></list-item><list-item id="u0015"><label>•</label><p>The core genome of malaria parasites is highly optimized for rapid host colonization</p></list-item><list-item id="u0020"><label>•</label><p>Essential parasite genes and pathways are identified for drug target prioritization</p></list-item><list-item id="u0025"><label>•</label><p>Low functional redundancy reflects the constant environment encountered by a parasite</p></list-item></list></p></abstract><abstract abstract-type="teaser" id="abs0025"><p>An in vivo genetic screen in a mouse model of malaria reveals the essential genes and pathways required by <italic>Plasmodium</italic> parasite, with a surprising two-thirds of the genome being required for normal parasite growth in the blood.</p></abstract><kwd-group id="kwrds0010"><title>Keywords</title><kwd>carcinoma-associated fibroblast (CAF)</kwd><kwd>tumor microenvironment</kwd><kwd>triple negative breast cancer</kwd><kwd>interferon</kwd><kwd>lncRNA</kwd><kwd>cancer inflammation</kwd><kwd>cancer immunology</kwd><kwd>myeloid cells</kwd><kwd>dendritic cells</kwd><kwd>radiation resistance</kwd></kwd-group></article-meta><notes><p id="misc0010">Published: July 13, 2017</p></notes></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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