Detection of human adaptation during the past 2000 years.
Identifieur interne : 001602 ( PubMed/Corpus ); précédent : 001601; suivant : 001603Detection of human adaptation during the past 2000 years.
Auteurs : Yair Field ; Evan A. Boyle ; Natalie Telis ; Ziyue Gao ; Kyle J. Gaulton ; David Golan ; Loic Yengo ; Ghislain Rocheleau ; Philippe Froguel ; Mark I. Mccarthy ; Jonathan K. PritchardSource :
- Science (New York, N.Y.) [ 1095-9203 ] ; 2016.
English descriptors
- KwdEn :
- Adaptation, Physiological (genetics), Eye Color (genetics), Gene Frequency, Genetic Loci, Genome, Human, Genome-Wide Association Study, Hair Color (genetics), Haplotypes, Humans (genetics), Lactase (genetics), Major Histocompatibility Complex (genetics), Pedigree, Selection, Genetic, United Kingdom.
- MESH :
- chemical , genetics : Lactase.
- genetics : Adaptation, Physiological, Eye Color, Hair Color, Humans, Major Histocompatibility Complex.
- Gene Frequency, Genetic Loci, Genome, Human, Genome-Wide Association Study, Haplotypes, Pedigree, Selection, Genetic, United Kingdom.
Abstract
Detection of recent natural selection is a challenging problem in population genetics. Here we introduce the singleton density score (SDS), a method to infer very recent changes in allele frequencies from contemporary genome sequences. Applied to data from the UK10K Project, SDS reflects allele frequency changes in the ancestors of modern Britons during the past ~2000 to 3000 years. We see strong signals of selection at lactase and the major histocompatibility complex, and in favor of blond hair and blue eyes. For polygenic adaptation, we find that recent selection for increased height has driven allele frequency shifts across most of the genome. Moreover, we identify shifts associated with other complex traits, suggesting that polygenic adaptation has played a pervasive role in shaping genotypic and phenotypic variation in modern humans.
DOI: 10.1126/science.aag0776
PubMed: 27738015
Links to Exploration step
pubmed:27738015Le document en format XML
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Boyle</name><affiliation><nlm:affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Telis, Natalie" sort="Telis, Natalie" uniqKey="Telis N" first="Natalie" last="Telis">Natalie Telis</name><affiliation><nlm:affiliation>Program in Biomedical Informatics, Stanford University, Stanford, CA 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Gao, Ziyue" sort="Gao, Ziyue" uniqKey="Gao Z" first="Ziyue" last="Gao">Ziyue Gao</name><affiliation><nlm:affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Gaulton, Kyle J" sort="Gaulton, Kyle J" uniqKey="Gaulton K" first="Kyle J" last="Gaulton">Kyle J. 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Boyle</name><affiliation><nlm:affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Telis, Natalie" sort="Telis, Natalie" uniqKey="Telis N" first="Natalie" last="Telis">Natalie Telis</name><affiliation><nlm:affiliation>Program in Biomedical Informatics, Stanford University, Stanford, CA 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Gao, Ziyue" sort="Gao, Ziyue" uniqKey="Gao Z" first="Ziyue" last="Gao">Ziyue Gao</name><affiliation><nlm:affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Gaulton, Kyle J" sort="Gaulton, Kyle J" uniqKey="Gaulton K" first="Kyle J" last="Gaulton">Kyle J. Gaulton</name><affiliation><nlm:affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Golan, David" sort="Golan, David" uniqKey="Golan D" first="David" last="Golan">David Golan</name><affiliation><nlm:affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Yengo, Loic" sort="Yengo, Loic" uniqKey="Yengo L" first="Loic" last="Yengo">Loic Yengo</name><affiliation><nlm:affiliation>Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Rocheleau, Ghislain" sort="Rocheleau, Ghislain" uniqKey="Rocheleau G" first="Ghislain" last="Rocheleau">Ghislain Rocheleau</name><affiliation><nlm:affiliation>Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Froguel, Philippe" sort="Froguel, Philippe" uniqKey="Froguel P" first="Philippe" last="Froguel">Philippe Froguel</name><affiliation><nlm:affiliation>Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Mccarthy, Mark I" sort="Mccarthy, Mark I" uniqKey="Mccarthy M" first="Mark I" last="Mccarthy">Mark I. Mccarthy</name><affiliation><nlm:affiliation>Wellcome Trust Center for Human Genetics, and Oxford Center for Diabetes Endocrinology and Metabolism, University of Oxford, Oxford, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Pritchard, Jonathan K" sort="Pritchard, Jonathan K" uniqKey="Pritchard J" first="Jonathan K" last="Pritchard">Jonathan K. Pritchard</name><affiliation><nlm:affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA. yairf@stanford.edu pritch@stanford.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Science (New York, N.Y.)</title><idno type="eISSN">1095-9203</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptation, Physiological (genetics)</term><term>Eye Color (genetics)</term><term>Gene Frequency</term><term>Genetic Loci</term><term>Genome, Human</term><term>Genome-Wide Association Study</term><term>Hair Color (genetics)</term><term>Haplotypes</term><term>Humans (genetics)</term><term>Lactase (genetics)</term><term>Major Histocompatibility Complex (genetics)</term><term>Pedigree</term><term>Selection, Genetic</term><term>United Kingdom</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Lactase</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adaptation, Physiological</term><term>Eye Color</term><term>Hair Color</term><term>Humans</term><term>Major Histocompatibility Complex</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Gene Frequency</term><term>Genetic Loci</term><term>Genome, Human</term><term>Genome-Wide Association Study</term><term>Haplotypes</term><term>Pedigree</term><term>Selection, Genetic</term><term>United Kingdom</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Detection of recent natural selection is a challenging problem in population genetics. Here we introduce the singleton density score (SDS), a method to infer very recent changes in allele frequencies from contemporary genome sequences. Applied to data from the UK10K Project, SDS reflects allele frequency changes in the ancestors of modern Britons during the past ~2000 to 3000 years. We see strong signals of selection at lactase and the major histocompatibility complex, and in favor of blond hair and blue eyes. For polygenic adaptation, we find that recent selection for increased height has driven allele frequency shifts across most of the genome. Moreover, we identify shifts associated with other complex traits, suggesting that polygenic adaptation has played a pervasive role in shaping genotypic and phenotypic variation in modern humans.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27738015</PMID><DateCreated><Year>2016</Year><Month>10</Month><Day>14</Day></DateCreated><DateCompleted><Year>2017</Year><Month>06</Month><Day>26</Day></DateCompleted><DateRevised><Year>2017</Year><Month>09</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-9203</ISSN><JournalIssue CitedMedium="Internet"><Volume>354</Volume><Issue>6313</Issue><PubDate><Year>2016</Year><Month>11</Month><Day>11</Day></PubDate></JournalIssue><Title>Science (New York, N.Y.)</Title><ISOAbbreviation>Science</ISOAbbreviation></Journal><ArticleTitle>Detection of human adaptation during the past 2000 years.</ArticleTitle><Pagination><MedlinePgn>760-764</MedlinePgn></Pagination><Abstract><AbstractText>Detection of recent natural selection is a challenging problem in population genetics. Here we introduce the singleton density score (SDS), a method to infer very recent changes in allele frequencies from contemporary genome sequences. Applied to data from the UK10K Project, SDS reflects allele frequency changes in the ancestors of modern Britons during the past ~2000 to 3000 years. We see strong signals of selection at lactase and the major histocompatibility complex, and in favor of blond hair and blue eyes. For polygenic adaptation, we find that recent selection for increased height has driven allele frequency shifts across most of the genome. Moreover, we identify shifts associated with other complex traits, suggesting that polygenic adaptation has played a pervasive role in shaping genotypic and phenotypic variation in modern humans.</AbstractText><CopyrightInformation>Copyright © 2016, American Association for the Advancement of Science.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Field</LastName><ForeName>Yair</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA. yairf@stanford.edu pritch@stanford.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boyle</LastName><ForeName>Evan A</ForeName><Initials>EA</Initials><AffiliationInfo><Affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Telis</LastName><ForeName>Natalie</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Program in Biomedical Informatics, Stanford University, Stanford, CA 94305, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>Ziyue</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gaulton</LastName><ForeName>Kyle J</ForeName><Initials>KJ</Initials><AffiliationInfo><Affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Wellcome Trust Center for Human Genetics, and Oxford Center for Diabetes Endocrinology and Metabolism, University of Oxford, Oxford, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Golan</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yengo</LastName><ForeName>Loic</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, F-59000 Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rocheleau</LastName><ForeName>Ghislain</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Froguel</LastName><ForeName>Philippe</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, F-59000 Lille, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Imperial College, Department of Genomics of Common Disease, London Hammersmith Hospital, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McCarthy</LastName><ForeName>Mark I</ForeName><Initials>MI</Initials><AffiliationInfo><Affiliation>Wellcome Trust Center for Human Genetics, and Oxford Center for Diabetes Endocrinology and Metabolism, University of Oxford, Oxford, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pritchard</LastName><ForeName>Jonathan K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>Department of Genetics, Stanford University, Stanford, CA 94305, USA. yairf@stanford.edu pritch@stanford.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biology, Stanford University, Stanford, CA, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>Dryad</DataBankName><AccessionNumberList><AccessionNumber>10.5061/dryad.kd58f</AccessionNumber></AccessionNumberList></DataBank></DataBankList><GrantList CompleteYN="Y"><Grant><GrantID>R01 MH101825</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 ES025009</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH084703</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><Agency>Howard Hughes Medical Institute</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 HG000044</GrantID><Acronym>HG</Acronym><Agency>NHGRI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>10</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Science</MedlineTA><NlmUniqueID>0404511</NlmUniqueID><ISSNLinking>0036-8075</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 3.2.1.108</RegistryNumber><NameOfSubstance UI="D043322">Lactase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2012 Oct 15;21(R1):R29-36</RefSource><PMID Version="1">22976473</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS Genet. 2014 Aug 07;10(8):e1004412</RefSource><PMID Version="1">25102153</PMID></CommentsCorrections><CommentsCorrections 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