The European wild boar was crossed with the domesticated Large White pig to genetically dissect phenotypic differences between these populations for growth and fat deposition. The most important effects were clustered on chromosome 4, with a single region accounting for a large part of the breed difference in growth rate, fatness, and length of the small intestine. The study is an advance in genome analyses and documents the usefulness of crosses between divergent outbred populations for the detection and characterization of quantitative trait loci. The genetic mapping of a major locus for fat deposition in the pig could have implications for understanding human obesity.
The change of phenotypic traits in domestic animals and crops as a response to selective breeding mimics the much slower evolutionary change in natural populations. Here, we describe that the dominant white phenotype in domestic pigs is caused by two mutations in the KIT gene encoding the mast/stem cell growth factor receptor (MGF), one gene duplication associated with a partially dominant phenotype and a splice mutation in one of the copies leading to the fully dominant allele. The splice mutation is a G to A substitution in the first nucleotide of intron 17 and leads to skipping of exon 17. The duplication is most likely a regulatory mutation affecting KIT expression, whereas the splice mutation is expected to cause a receptor with impaired or absent tyrosine kinase activity. Immunocytochemistry showed that this variant form is expressed in
In 1995, Edfors-Lilja and coworkers mapped the locus for the E. coli K88ab (F4ab) and K88ac (F4ac) intestinal receptor to pig chromosome 13 (SSC13). Using the same family material we have refined the map position to a region between the microsatellite markers Sw207 and Sw225. Primers from these markers were used to screen a pig BAC library and the positive clones were used for fluorescent in situ hybridization (FISH) analysis. The results of the FISH analysis helped to propose a candidate gene region in the SSC13q41→q44 interval. Shotgun sequencing of the FISH-mapped BAC clones revealed that the candidate region contains an evolutionary breakpoint between human and pig. In order to further characterise the rearrangements between SSC13 and human chromosome 3 (HSA3), detailed gene mapping of SSC13 was carried out. Based on this mapping data we have constructed a detailed comparative map between SSC13 and HSA3. Two candidate regions on human chromosome 3 have been identified that are likely to harbour the human homologue of the gene responsible for susceptibility towards E. coli F4ab/ac diarrhoea in pigs.
A genome wide search in European Wild Boar x Swedish Yorkshire (W x Y) inter-cross pigs has earlier identified quantitative trait loci (QTL) for leucocyte number and function on porcine chromosomes 1 and 8 (SSC 1 and 8). To verify the involvement of these chromosomal regions in the regulation of haematocrit (Hem) and haemoglobin (Hb) levels, leucocyte numbers and in vitro leukocyte functions (mitogen induced proliferation and IL-2 production, virus induced interferon-alpha production and neutrophil phagocytosis), animals of different genetic backgrounds were analysed. The animals comprised a back-cross sire family (n=47) of W x Y pigs and six crossbred [Y x Landrace (L)] sire families (n=191). They were genotyped for 16 genetic markers and an interval analysis was performed. On SSC1, a QTL close to S0082 on the q-arm that influenced numbers of white blood cells in L x Y pigs and numbers of band neutrophils and CD8(+) cells in W x Y pigs was identified (P
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