Human-chimpanzee DNA sequence variation in the four major genes of the renin angiotensin system
Identifieur interne : 005C60 ( PascalFrancis/Checkpoint ); précédent : 005C59; suivant : 005C61Human-chimpanzee DNA sequence variation in the four major genes of the renin angiotensin system
Auteurs : Cécile Dufour [France] ; Didier Casane [France] ; Derek Denton [Australie] ; Jean Wickings [Gabon] ; Pierre Corvol [France] ; Xavier Jeunemaitre [France]Source :
- Genomics : (San Diego, CA) [ 0888-7543 ] ; 2000.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
Abstract
The renin angiotensin system (RAS) is involved in blood pressure control and water/sodium metabolism. The genes encoding the proteins of this system are candidate genes for essential hypertension. The RAS involves four main molecules: angiotensinogen, renin, angiotensin I-converting enzyme, and the angiotensin II type 1 receptor (encoded by the genes AGT, REN, DCP1, and AGTR1, respectively). We performed a molecular screening over 17,037 bp of the coding and 5' and 3' untranslated regions of these genes, from three to six common chimpanzees. We identified 44 single-nucleotide polymorphisms (SNPs) in chimpanzee samples, including 18 coding-region SNPs, 5 of which led to an amino acid replacement. We observed common and different features at various sites (synonymous, nonsynonymous, and noncoding) within and between the four chimpanzee genes: (1) the nucleotide diversity at noncoding sites was similar; (2) the nucleotide diversity at nonsynonymous sites was low, probably reflecting purifying selection, except for the AGT gene; (3) the nucleotide diversity at synonymous sites, which was dependent on the G+C content at the third position of the codon, was high, except for the AGTR1 gene. Comparison of the chimpanzee SNPs with those previously reported for humans identified 119 sites with fixed differences (including 62 coding sites, 17 of which resulted in amino acid differences between the species). Analysis of polymorphism within species and divergence between species shed light on the evolutionary constraints on these genes. In particular, comparison of the pattern of mutation at polymorphic and fixed sites between humans and chimpanzees suggested that the high G+C content of the DCP1 gene was maintained by positive selection at its silent sites. Finally, we propose 68 ancestral alleles for the human RAS genes and discuss the implications for their use in future hypertension-susceptibility association studies.
Affiliations:
- Australie, France, Gabon
- Victoria (État), Île-de-France
- Melbourne, Orsay, Paris
- Université Paris-Sud, Université de Melbourne
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la Recherche Médicale U36, 3, rue d'Ulm</s1><s2>75005 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Casane, Didier" sort="Casane, Didier" uniqKey="Casane D" first="Didier" last="Casane">Didier Casane</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Equipe "phylogénie et évolution moléculaires," UPRESA CNRS 8080, Bâtiment 444, Université Paris-Sud</s1><s2>91405 Orsay</s2><s3>FRA</s3><sZ>2 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Orsay</settlement><settlement type="city">Orsay</settlement></placeName><orgName type="university">Université Paris-Sud</orgName></affiliation></author><author><name sortKey="Denton, Derek" sort="Denton, Derek" uniqKey="Denton D" first="Derek" last="Denton">Derek Denton</name><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne</s1><s2>Parkville, Victoria 3052</s2><s3>AUS</s3><sZ>3 aut.</sZ></inist:fA14><country>Australie</country><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName><orgName type="university">Université de Melbourne</orgName></affiliation></author><author><name sortKey="Wickings, Jean" sort="Wickings, Jean" uniqKey="Wickings J" first="Jean" last="Wickings">Jean Wickings</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Centre International de Recherche Médicale, BP 769</s1><s2>Franceville</s2><s3>GAB</s3><sZ>4 aut.</sZ></inist:fA14><country>Gabon</country><wicri:noRegion>Franceville</wicri:noRegion></affiliation></author><author><name sortKey="Corvol, Pierre" sort="Corvol, Pierre" uniqKey="Corvol P" first="Pierre" last="Corvol">Pierre Corvol</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Pathologie Vasculaire et Endocrinologie Rénale, Collège de France, Chaire de Médecine Expérimentale et d'Endocrinologie Rénale, Institut National de la Santé et de la Recherche Médicale U36, 3, rue d'Ulm</s1><s2>75005 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>75005 Paris</wicri:noRegion><placeName><settlement type="city">Paris</settlement><region type="région" nuts="2">Île-de-France</region></placeName></affiliation></author><author><name sortKey="Jeunemaitre, Xavier" sort="Jeunemaitre, Xavier" uniqKey="Jeunemaitre X" first="Xavier" last="Jeunemaitre">Xavier Jeunemaitre</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Pathologie Vasculaire et Endocrinologie Rénale, Collège de France, Chaire de Médecine Expérimentale et d'Endocrinologie Rénale, Institut National de la Santé et de la Recherche Médicale U36, 3, rue d'Ulm</s1><s2>75005 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>75005 Paris</wicri:noRegion><placeName><settlement type="city">Paris</settlement><region type="région" nuts="2">Île-de-France</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Genomics : (San Diego, CA)</title><title level="j" type="abbreviated">Genomics : (S. Diego CA)</title><idno type="ISSN">0888-7543</idno><imprint><date when="2000">2000</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Genomics : (San Diego, CA)</title><title level="j" type="abbreviated">Genomics : (S. Diego CA)</title><idno type="ISSN">0888-7543</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Blood pressure</term><term>Gene</term><term>Genetic variability</term><term>Human</term><term>Hypertension</term><term>Interspecific comparison</term><term>Intraspecific comparison</term><term>Molecular evolution</term><term>Pan troglodytes</term><term>Regulation(control)</term><term>Renin angiotensin system</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Homme</term><term>Pan troglodytes</term><term>Système renin angiotensine</term><term>Gène</term><term>Variabilité génétique</term><term>Evolution moléculaire</term><term>Comparaison intraspécifique</term><term>Comparaison interspécifique</term><term>Pression sanguine</term><term>Hypertension artérielle</term><term>Régulation</term><term>Polymorphisme mononucléotide</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The renin angiotensin system (RAS) is involved in blood pressure control and water/sodium metabolism. The genes encoding the proteins of this system are candidate genes for essential hypertension. The RAS involves four main molecules: angiotensinogen, renin, angiotensin I-converting enzyme, and the angiotensin II type 1 receptor (encoded by the genes AGT, REN, DCP1, and AGTR1, respectively). We performed a molecular screening over 17,037 bp of the coding and 5' and 3' untranslated regions of these genes, from three to six common chimpanzees. We identified 44 single-nucleotide polymorphisms (SNPs) in chimpanzee samples, including 18 coding-region SNPs, 5 of which led to an amino acid replacement. We observed common and different features at various sites (synonymous, nonsynonymous, and noncoding) within and between the four chimpanzee genes: (1) the nucleotide diversity at noncoding sites was similar; (2) the nucleotide diversity at nonsynonymous sites was low, probably reflecting purifying selection, except for the AGT gene; (3) the nucleotide diversity at synonymous sites, which was dependent on the G+C content at the third position of the codon, was high, except for the AGTR1 gene. Comparison of the chimpanzee SNPs with those previously reported for humans identified 119 sites with fixed differences (including 62 coding sites, 17 of which resulted in amino acid differences between the species). Analysis of polymorphism within species and divergence between species shed light on the evolutionary constraints on these genes. In particular, comparison of the pattern of mutation at polymorphic and fixed sites between humans and chimpanzees suggested that the high G+C content of the DCP1 gene was maintained by positive selection at its silent sites. Finally, we propose 68 ancestral alleles for the human RAS genes and discuss the implications for their use in future hypertension-susceptibility association studies.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0888-7543</s0></fA01><fA03 i2="1"><s0>Genomics : (S. Diego CA)</s0></fA03><fA05><s2>69</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Human-chimpanzee DNA sequence variation in the four major genes of the renin angiotensin system</s1></fA08><fA11 i1="01" i2="1"><s1>DUFOUR (Cécile)</s1></fA11><fA11 i1="02" i2="1"><s1>CASANE (Didier)</s1></fA11><fA11 i1="03" i2="1"><s1>DENTON (Derek)</s1></fA11><fA11 i1="04" i2="1"><s1>WICKINGS (Jean)</s1></fA11><fA11 i1="05" i2="1"><s1>CORVOL (Pierre)</s1></fA11><fA11 i1="06" i2="1"><s1>JEUNEMAITRE (Xavier)</s1></fA11><fA14 i1="01"><s1>Pathologie Vasculaire et Endocrinologie Rénale, Collège de France, Chaire de Médecine Expérimentale et d'Endocrinologie Rénale, Institut National de la Santé et de la Recherche Médicale U36, 3, rue d'Ulm</s1><s2>75005 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="02"><s1>Equipe "phylogénie et évolution moléculaires," UPRESA CNRS 8080, Bâtiment 444, Université Paris-Sud</s1><s2>91405 Orsay</s2><s3>FRA</s3><sZ>2 aut.</sZ></fA14><fA14 i1="03"><s1>Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne</s1><s2>Parkville, Victoria 3052</s2><s3>AUS</s3><sZ>3 aut.</sZ></fA14><fA14 i1="04"><s1>Centre International de Recherche Médicale, BP 769</s1><s2>Franceville</s2><s3>GAB</s3><sZ>4 aut.</sZ></fA14><fA20><s1>14-26</s1></fA20><fA21><s1>2000</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>21389</s2><s5>354000092666030020</s5></fA43><fA44><s0>0000</s0><s1>© 2001 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>01-0049610</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Genomics : (San Diego, CA)</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>The renin angiotensin system (RAS) is involved in blood pressure control and water/sodium metabolism. The genes encoding the proteins of this system are candidate genes for essential hypertension. The RAS involves four main molecules: angiotensinogen, renin, angiotensin I-converting enzyme, and the angiotensin II type 1 receptor (encoded by the genes AGT, REN, DCP1, and AGTR1, respectively). We performed a molecular screening over 17,037 bp of the coding and 5' and 3' untranslated regions of these genes, from three to six common chimpanzees. We identified 44 single-nucleotide polymorphisms (SNPs) in chimpanzee samples, including 18 coding-region SNPs, 5 of which led to an amino acid replacement. We observed common and different features at various sites (synonymous, nonsynonymous, and noncoding) within and between the four chimpanzee genes: (1) the nucleotide diversity at noncoding sites was similar; (2) the nucleotide diversity at nonsynonymous sites was low, probably reflecting purifying selection, except for the AGT gene; (3) the nucleotide diversity at synonymous sites, which was dependent on the G+C content at the third position of the codon, was high, except for the AGTR1 gene. Comparison of the chimpanzee SNPs with those previously reported for humans identified 119 sites with fixed differences (including 62 coding sites, 17 of which resulted in amino acid differences between the species). Analysis of polymorphism within species and divergence between species shed light on the evolutionary constraints on these genes. In particular, comparison of the pattern of mutation at polymorphic and fixed sites between humans and chimpanzees suggested that the high G+C content of the DCP1 gene was maintained by positive selection at its silent sites. Finally, we propose 68 ancestral alleles for the human RAS genes and discuss the implications for their use in future hypertension-susceptibility association studies.</s0></fC01><fC02 i1="01" i2="X"><s0>002A07C01B</s0></fC02><fC02 i1="02" i2="X"><s0>002A07C03</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Homme</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Human</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Hombre</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Pan troglodytes</s0><s2>NS</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Pan troglodytes</s0><s2>NS</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Pan troglodytes</s0><s2>NS</s2><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Système renin angiotensine</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Renin angiotensin system</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Sistema renin angiotensina</s0><s5>05</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Gène</s0><s5>06</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Gene</s0><s5>06</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Gen</s0><s5>06</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Variabilité génétique</s0><s5>07</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Genetic variability</s0><s5>07</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Variabilidad genética</s0><s5>07</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Evolution moléculaire</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Molecular evolution</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Evolución molecular</s0><s5>09</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Comparaison intraspécifique</s0><s5>10</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Intraspecific comparison</s0><s5>10</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Comparación intraespecífica</s0><s5>10</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Comparaison interspécifique</s0><s5>11</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Interspecific comparison</s0><s5>11</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Comparación interespecífica</s0><s5>11</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Pression sanguine</s0><s5>13</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Blood pressure</s0><s5>13</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Presión sanguínea</s0><s5>13</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Hypertension artérielle</s0><s5>14</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Hypertension</s0><s5>14</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Hipertensión arterial</s0><s5>14</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Régulation</s0><s5>39</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Regulation(control)</s0><s5>39</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Regulación</s0><s5>39</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Polymorphisme mononucléotide</s0><s4>INC</s4><s5>91</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Simioidea</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Simioidea</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Simioidea</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>029</s1></fN21></pA></standard></inist><affiliations><list><country><li>Australie</li><li>France</li><li>Gabon</li></country><region><li>Victoria (État)</li><li>Île-de-France</li></region><settlement><li>Melbourne</li><li>Orsay</li><li>Paris</li></settlement><orgName><li>Université Paris-Sud</li><li>Université de Melbourne</li></orgName></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Dufour, Cecile" sort="Dufour, Cecile" uniqKey="Dufour C" first="Cécile" last="Dufour">Cécile Dufour</name></region><name sortKey="Casane, Didier" sort="Casane, Didier" uniqKey="Casane D" first="Didier" last="Casane">Didier Casane</name><name sortKey="Corvol, Pierre" sort="Corvol, Pierre" uniqKey="Corvol P" first="Pierre" last="Corvol">Pierre Corvol</name><name sortKey="Jeunemaitre, Xavier" sort="Jeunemaitre, Xavier" uniqKey="Jeunemaitre X" first="Xavier" last="Jeunemaitre">Xavier Jeunemaitre</name></country><country name="Australie"><region name="Victoria (État)"><name sortKey="Denton, Derek" sort="Denton, Derek" uniqKey="Denton D" first="Derek" last="Denton">Derek Denton</name></region></country><country name="Gabon"><noRegion><name sortKey="Wickings, Jean" sort="Wickings, Jean" uniqKey="Wickings J" first="Jean" last="Wickings">Jean Wickings</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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