Sex-Specific Regulation of Mitochondrial DNA Levels: Genome-Wide Linkage Analysis to Identify Quantitative Trait Loci
Identifieur interne : 001068 ( Main/Curation ); précédent : 001067; suivant : 001069Sex-Specific Regulation of Mitochondrial DNA Levels: Genome-Wide Linkage Analysis to Identify Quantitative Trait Loci
Auteurs : Sonia L Pez [Espagne] ; Alfonso Buil [Espagne] ; Juan Carlos Souto [Espagne] ; Jordi Casademont [Espagne] ; John Blangero [États-Unis] ; Angel Martinez-Perez [Espagne] ; Jordi Fontcuberta [Espagne] ; Mark Lathrop [France] ; Laura Almasy [États-Unis] ; Jose Manuel Soria [Espagne]Source :
- PLoS ONE [ 1932-6203 ] ; 2012.
Abstract
Altered mitochondrial DNA (mtDNA) levels have been associated with common diseases in humans. We investigated the genetic mechanism that controls mtDNA levels using genome-wide linkage analyses in families from the Genetic Analysis of Idiopathic Thrombophilia Project (GAIT). We measure mtDNA levels by quantitative real-time PCR in 386 subjects from 21 extended Spanish families. A variance component linkage method using 485 microsatellites was conducted to evaluate linkage and to detect quantitative trait loci (QTLs) involved in the control of mtDNA levels. The heritalibility of mtDNA levels was 0.33 (p = 1.82e-05). We identified a QTL on Chromosome 2 (LOD = 2.21) using all of the subjects, independently on their sex. When females and males were analysed separately, three QTLs were identified. Females showed the same QTL on Chromosome 2 (LOD = 3.09), indicating that the QTL identified in the analysis using all of the subjects was a strong female QTL, and another one on Chromosome 3 (LOD = 2.67), whereas in males a QTL was identified on Chromosome 1 (LOD = 2.81). These QTLs were fine-mapped to find associations with mtDNA levels. The most significant SNP association was for the rs10888838 on Chromosome 1 in males. This SNP mapped to the gene
Url:
DOI: 10.1371/journal.pone.0042711
PubMed: 22916149
PubMed Central: 3423410
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uniqKey="Almasy L" first="Laura" last="Almasy">Laura Almasy</name><affiliation wicri:level="2"><nlm:aff id="aff4"><addr-line>Department of Population Genetics, Texas Biomedical Research Institute, San Antonio, Texas, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Population Genetics, Texas Biomedical Research Institute, San Antonio, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Soria, Jose Manuel" sort="Soria, Jose Manuel" uniqKey="Soria J" first="Jose Manuel" last="Soria">Jose Manuel Soria</name><affiliation wicri:level="3"><nlm:aff id="aff1"><addr-line>Unit of Genomic of Complex Diseases, Institute of Biomedical Research of Hospital de la Santa Creu i Sant Pau, Barcelona, Spain</addr-line></nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea>Unit of Genomic of Complex Diseases, Institute of Biomedical Research of Hospital de la Santa Creu i Sant Pau, Barcelona</wicri:regionArea><placeName><settlement type="city">Barcelone</settlement><region nuts="2" type="region">Catalogne</region></placeName></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Altered mitochondrial DNA (mtDNA) levels have been associated with common diseases in humans. We investigated the genetic mechanism that controls mtDNA levels using genome-wide linkage analyses in families from the Genetic Analysis of Idiopathic Thrombophilia Project (GAIT). We measure mtDNA levels by quantitative real-time PCR in 386 subjects from 21 extended Spanish families. A variance component linkage method using 485 microsatellites was conducted to evaluate linkage and to detect quantitative trait loci (QTLs) involved in the control of mtDNA levels. The heritalibility of mtDNA levels was 0.33 (p = 1.82e-05). We identified a QTL on Chromosome 2 (LOD = 2.21) using all of the subjects, independently on their sex. When females and males were analysed separately, three QTLs were identified. Females showed the same QTL on Chromosome 2 (LOD = 3.09), indicating that the QTL identified in the analysis using all of the subjects was a strong female QTL, and another one on Chromosome 3 (LOD = 2.67), whereas in males a QTL was identified on Chromosome 1 (LOD = 2.81). These QTLs were fine-mapped to find associations with mtDNA levels. The most significant SNP association was for the rs10888838 on Chromosome 1 in males. This SNP mapped to the gene <italic>MRPL37</italic>, involved in mitochondrial protein translation. The rs2140855 on Chromosome 2 showed association in the analysis using all of the subjects. It was near the gene <italic>CMPK2</italic>, which encodes a mitochondrial enzyme of the salvage pathway of deoxyribonucleotide synthesis. Our results provide evidence of a sex-specific genetic mechanism for the control of mtDNA levels and provide a framework to identify new genes that influence mtDNA levels.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Kushnareva, Y" uniqKey="Kushnareva Y">Y Kushnareva</name></author><author><name sortKey="Newmeyer, Dd" uniqKey="Newmeyer D">DD Newmeyer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yu, X" uniqKey="Yu X">X Yu</name></author><author><name sortKey="Koczan, D" uniqKey="Koczan D">D Koczan</name></author><author><name sortKey="Sulonen, Am" uniqKey="Sulonen A">AM Sulonen</name></author><author><name sortKey="Akkad, Da" uniqKey="Akkad D">DA Akkad</name></author><author><name sortKey="Kroner, A" uniqKey="Kroner A">A Kroner</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Czarnecka, Am" uniqKey="Czarnecka A">AM Czarnecka</name></author><author><name 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