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Dissection of genetic factors modulating fetal growth in cattle indicates a substantial role of the non-SMC condensin I complex, subunit G (NCAPG) gene.
Genetics 183, 951-964 (2009)
Verlagsversion Forschungsdaten DOI
The increasing evidence of fetal developmental effects on postnatal life, the Still unknown fetal growth mechanisms impairing offspring generated by somatic nuclear transfer techniques, and the impact on stillbirth and dystocia in conventional reproduction have generated increasing attention toward mammalian fetal growth. We identified a highly significant quantitative trait locus (QTL) affecting fetal growth on bovine chromosome 6 in a specific resource Population, which was set tip by consistent rise of embryo transfer and foster mothers and, thus, enabled dissection of fetal-specific genetic components of fetal growth. Merging our data with results from other cattle populations differing in historical and geographical origin and with comparative data from human whole-genome association mapping suggests that a nonsynonymous polymorphism in the non-SMC condensin I complex, Subunit G (NCAPG) gene, NCAPG c.1326T>G, is the potential cause of tire identified QTL resulting in divergent bovine fetal growth. NCAPG gene expression data in fetal placentomes with different NCAPG c.1326T>G genotypes, which are in line with recent results about differential NCAPG expression in placentomes from studies on assisted reproduction techniques, indicate that the NCAPG locus may give valuable information on the specific mechanisms regulating fetal growth in mammals.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Quantitative trait loci; Whole-genome scan; Functional traits; Chromosome condensation; Calving difficulty; Gestation length; Osteopontin gene; Nuclear transfer; Holstein cattle; Birth-weight
ISSN (print) / ISBN 0016-6731
Quellenangaben Band: 183, Heft: 3, Seiten: 951-964
Verlag Genetics Society of America
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology I (EPI1)