Genomic convergence to identify candidate genes for Parkinson disease: SAGE analysis of the substantia nigra.
Identifieur interne : 003017 ( PubMed/Curation ); précédent : 003016; suivant : 003018Genomic convergence to identify candidate genes for Parkinson disease: SAGE analysis of the substantia nigra.
Auteurs : Maher A. Noureddine [États-Unis] ; Yi-Ju Li ; Joelle M. Van Der Walt ; Robert Walters ; Rita M. Jewett ; Hong Xu ; Tianyuan Wang ; Jeffrey W. Walter ; Burton L. Scott ; Christine Hulette ; Don Schmechel ; Judith E. Stenger ; Fred Dietrich ; Jeffery M. Vance ; Michael A. HauserSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, DNA, Mitochondrial (genetics), Expressed Sequence Tags (metabolism), Female, Gene Expression, Gene Library, Genetic Linkage (genetics), Genetic Predisposition to Disease, Genetic Techniques, Humans, Male, Oligonucleotide Array Sequence Analysis (methods), Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (pathology), Proteomics (methods), RNA, Messenger (genetics), RNA, Messenger (metabolism), Risk Factors, Substantia Nigra (metabolism), Substantia Nigra (pathology).
- MESH :
- chemical , genetics : DNA, Mitochondrial, RNA, Messenger.
- genetics : Genetic Linkage, Parkinson Disease.
- metabolism : Expressed Sequence Tags, Parkinson Disease, RNA, Messenger, Substantia Nigra.
- methods : Oligonucleotide Array Sequence Analysis, Proteomics.
- pathology : Parkinson Disease, Substantia Nigra.
- Aged, Aged, 80 and over, Female, Gene Expression, Gene Library, Genetic Predisposition to Disease, Genetic Techniques, Humans, Male, Risk Factors.
Abstract
Genomic convergence is a multistep approach that combines gene expression with genomic linkage to identify and prioritize susceptibility genes for complex disease. As a first step, we previously performed linkage analysis on 174 multiplex Parkinson's disease (PD) families, identifying five peaks for PD risk and two for genes affecting age at onset (AAO) in PD [Hauser et al., Hum Mol Genet 2003;12:671-677]. We report here the next step: serial analysis of gene expression [SAGE; Scott et al., JAMA 2001;286:2239-2242] to analyze substantia nigra tissue from three PD patients and two age-matched controls. We find 933 differentially expressed genes (P<0.05) between PD and controls, but of these, only 50 genes represented by unique SAGE tags map within our previously described PD linkage regions. Furthermore, genes encoded by mitochondrial DNA are expressed 1.5-fold higher in PD patients versus controls, without an increase in the corresponding nuclear-encoded mitochondrial components, suggesting an increase in mtDNA genomes in PD or a disjunction with nuclear expression. The next step in the genomic convergence process will be to screen these 50 high-quality candidate genes for association with PD risk susceptibility and genetic effects on AAO.
DOI: 10.1002/mds.20573
PubMed: 15966006
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Noureddine</name><affiliation wicri:level="1"><nlm:affiliation>Center for Human Genetics, Duke University, Durham, North Carolina 27710-2903, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Human Genetics, Duke University, Durham, North Carolina 27710-2903</wicri:regionArea></affiliation></author><author><name sortKey="Li, Yi Ju" sort="Li, Yi Ju" uniqKey="Li Y" first="Yi-Ju" last="Li">Yi-Ju Li</name></author><author><name sortKey="Van Der Walt, Joelle M" sort="Van Der Walt, Joelle M" uniqKey="Van Der Walt J" first="Joelle M" last="Van Der Walt">Joelle M. Van Der Walt</name></author><author><name sortKey="Walters, Robert" sort="Walters, Robert" uniqKey="Walters R" first="Robert" last="Walters">Robert Walters</name></author><author><name sortKey="Jewett, Rita M" sort="Jewett, Rita M" uniqKey="Jewett R" first="Rita M" last="Jewett">Rita M. Jewett</name></author><author><name sortKey="Xu, Hong" sort="Xu, Hong" uniqKey="Xu H" first="Hong" last="Xu">Hong Xu</name></author><author><name sortKey="Wang, Tianyuan" sort="Wang, Tianyuan" uniqKey="Wang T" first="Tianyuan" last="Wang">Tianyuan Wang</name></author><author><name sortKey="Walter, Jeffrey W" sort="Walter, Jeffrey W" uniqKey="Walter J" first="Jeffrey W" last="Walter">Jeffrey W. Walter</name></author><author><name sortKey="Scott, Burton L" sort="Scott, Burton L" uniqKey="Scott B" first="Burton L" last="Scott">Burton L. Scott</name></author><author><name sortKey="Hulette, Christine" sort="Hulette, Christine" uniqKey="Hulette C" first="Christine" last="Hulette">Christine Hulette</name></author><author><name sortKey="Schmechel, Don" sort="Schmechel, Don" uniqKey="Schmechel D" first="Don" last="Schmechel">Don Schmechel</name></author><author><name sortKey="Stenger, Judith E" sort="Stenger, Judith E" uniqKey="Stenger J" first="Judith E" last="Stenger">Judith E. Stenger</name></author><author><name sortKey="Dietrich, Fred" sort="Dietrich, Fred" uniqKey="Dietrich F" first="Fred" last="Dietrich">Fred Dietrich</name></author><author><name sortKey="Vance, Jeffery M" sort="Vance, Jeffery M" uniqKey="Vance J" first="Jeffery M" last="Vance">Jeffery M. Vance</name></author><author><name sortKey="Hauser, Michael A" sort="Hauser, Michael A" uniqKey="Hauser M" first="Michael A" last="Hauser">Michael A. Hauser</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>DNA, Mitochondrial (genetics)</term><term>Expressed Sequence Tags (metabolism)</term><term>Female</term><term>Gene Expression</term><term>Gene Library</term><term>Genetic Linkage (genetics)</term><term>Genetic Predisposition to Disease</term><term>Genetic Techniques</term><term>Humans</term><term>Male</term><term>Oligonucleotide Array Sequence Analysis (methods)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Proteomics (methods)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Risk Factors</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA, Mitochondrial</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Genetic Linkage</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Expressed Sequence Tags</term><term>Parkinson Disease</term><term>RNA, Messenger</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Oligonucleotide Array Sequence Analysis</term><term>Proteomics</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Gene Expression</term><term>Gene Library</term><term>Genetic Predisposition to Disease</term><term>Genetic Techniques</term><term>Humans</term><term>Male</term><term>Risk Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Genomic convergence is a multistep approach that combines gene expression with genomic linkage to identify and prioritize susceptibility genes for complex disease. As a first step, we previously performed linkage analysis on 174 multiplex Parkinson's disease (PD) families, identifying five peaks for PD risk and two for genes affecting age at onset (AAO) in PD [Hauser et al., Hum Mol Genet 2003;12:671-677]. We report here the next step: serial analysis of gene expression [SAGE; Scott et al., JAMA 2001;286:2239-2242] to analyze substantia nigra tissue from three PD patients and two age-matched controls. We find 933 differentially expressed genes (P<0.05) between PD and controls, but of these, only 50 genes represented by unique SAGE tags map within our previously described PD linkage regions. Furthermore, genes encoded by mitochondrial DNA are expressed 1.5-fold higher in PD patients versus controls, without an increase in the corresponding nuclear-encoded mitochondrial components, suggesting an increase in mtDNA genomes in PD or a disjunction with nuclear expression. The next step in the genomic convergence process will be to screen these 50 high-quality candidate genes for association with PD risk susceptibility and genetic effects on AAO.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">15966006</PMID><DateCreated><Year>2005</Year><Month>10</Month><Day>11</Day></DateCreated><DateCompleted><Year>2006</Year><Month>02</Month><Day>16</Day></DateCompleted><DateRevised><Year>2010</Year><Month>11</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>20</Volume><Issue>10</Issue><PubDate><Year>2005</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Genomic convergence to identify candidate genes for Parkinson disease: SAGE analysis of the substantia nigra.</ArticleTitle><Pagination><MedlinePgn>1299-309</MedlinePgn></Pagination><Abstract><AbstractText>Genomic convergence is a multistep approach that combines gene expression with genomic linkage to identify and prioritize susceptibility genes for complex disease. As a first step, we previously performed linkage analysis on 174 multiplex Parkinson's disease (PD) families, identifying five peaks for PD risk and two for genes affecting age at onset (AAO) in PD [Hauser et al., Hum Mol Genet 2003;12:671-677]. We report here the next step: serial analysis of gene expression [SAGE; Scott et al., JAMA 2001;286:2239-2242] to analyze substantia nigra tissue from three PD patients and two age-matched controls. We find 933 differentially expressed genes (P<0.05) between PD and controls, but of these, only 50 genes represented by unique SAGE tags map within our previously described PD linkage regions. Furthermore, genes encoded by mitochondrial DNA are expressed 1.5-fold higher in PD patients versus controls, without an increase in the corresponding nuclear-encoded mitochondrial components, suggesting an increase in mtDNA genomes in PD or a disjunction with nuclear expression. The next step in the genomic convergence process will be to screen these 50 high-quality candidate genes for association with PD risk susceptibility and genetic effects on AAO.</AbstractText><CopyrightInformation>Copyright (c) 2005 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Noureddine</LastName><ForeName>Maher A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Center for Human Genetics, Duke University, Durham, North Carolina 27710-2903, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yi-Ju</ForeName><Initials>YJ</Initials></Author><Author ValidYN="Y"><LastName>van der Walt</LastName><ForeName>Joelle M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Walters</LastName><ForeName>Robert</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Jewett</LastName><ForeName>Rita M</ForeName><Initials>RM</Initials></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Hong</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Tianyuan</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Walter</LastName><ForeName>Jeffrey W</ForeName><Initials>JW</Initials></Author><Author ValidYN="Y"><LastName>Scott</LastName><ForeName>Burton L</ForeName><Initials>BL</Initials></Author><Author ValidYN="Y"><LastName>Hulette</LastName><ForeName>Christine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Schmechel</LastName><ForeName>Don</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Stenger</LastName><ForeName>Judith E</ForeName><Initials>JE</Initials></Author><Author ValidYN="Y"><LastName>Dietrich</LastName><ForeName>Fred</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Vance</LastName><ForeName>Jeffery M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Hauser</LastName><ForeName>Michael A</ForeName><Initials>MA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>ES00372</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS39764</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 AG05128</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004272">DNA, Mitochondrial</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000369">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004272">DNA, Mitochondrial</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020224">Expressed Sequence Tags</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D015870">Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D015723">Gene Library</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008040">Genetic Linkage</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020022">Genetic Predisposition to Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005821">Genetic Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020411">Oligonucleotide Array Sequence Analysis</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D040901">Proteomics</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012333">RNA, Messenger</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012307">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013378">Substantia Nigra</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>6</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>2</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>6</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.20573</ArticleId><ArticleId 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