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1 Research Center for Exercise and Health, Faculty of Kinesiology and Rehabilitation Sciences, Katholieke Universiteit Leuven, Leuven, Belgium
2 Drug Discovery, Johnson & Johnson Pharmaceutical Research and Development, Beerse, Belgium; Department of Population Genetics, Genomics and Bio-informatics, Universiteit Maastricht, Maastricht, The Netherlands
3 Department of Human Genetics, Faculty of Medicine, Katholieke Universiteit Leuven, Leuven, Belgium; Department of Population Genetics, Genomics and Bio-informatics, Universiteit Maastricht, Maastricht, The Netherlands
* To whom correspondence should be addressed. E-mail: martine.thomis{at}faber.kuleuven.be.
This study reports the results of a multipoint linkage study that aims to unravel the genetic basis of muscle strength and muscle mass in humans. Myostatin (GDF8) is known to be a strong inhibitor of muscle growth in animals. However, studies examining human myostatin polymorphisms are rare and are limited to the GDF8 gene itself. Here, the contribution to isometric and concentric knee strength of nine key proteins, involved in the myostatin pathway, is studied in a non-parametric multi-point linkage analysis by means of a variance components and regression method. A sample of 367 healthy young male siblings was phenotyped on an isokinetic dynamometer and genotyped for markers of the myostatin pathway genes. Three of the loci were found significantly linked with a QTL for knee muscle strength. First, D13S1303 showed replication of an explorative single-point linkage study with a maximum LOD score of 2.7 (P = 0.0002). Second, maximum LOD scores of 3.4 (P = 0.00004) and 3.3 (P = 0.00005) were observed for markers D12S1042 and D12S85 respectively at 12q12-14. Finally, marker D12S78 showed a LOD score of 2.7 at 12q22-23. We conclude that several genes involved in the myostatin pathway, but not the myostatin gene itself, are important QTLs for human muscle strength. An additional set of valuable candidate genes was found in the chromosome 12 and 13 genomic regions that were not part of the myostatin pathway.
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