Bovine umbilical hernia maps to the centromeric end of Bos taurus autosome 8.

Twelve bull calves were produced by mating elite Israeli cows to "Glenhapton Enhancer", a Canadian Holstein bull. The frequency of umbilical hernia (UH) in the progeny of the sons ranged from 1 to 21%, consistent with the hypothesis that Enhancer is the carrier of major dominant or codominant gene with partial penetrance for UH. Five sons of Enhancer produced progeny with >10% frequency of UH including sire 3259, whereas progeny of three sons had <3% UH. A total of 116 grand-progeny of Enhancer, all progeny of 3259, were genotyped for 59 microsatellites spanning the 29 bovine autosomes. Of these offspring, 41 were affected. Significant differences in paternal allele frequencies between the affected and unaffected progeny groups were found for marker BMS1591 on bovine chromosome 8 (BTA8). The UH-associated paternal allele originated from Enhancer. The chromosomal segment associated with UH was more precisely mapped between UWCA47, on the centromeric end of BTA8 and RM321, 12 cM from the centromere. A maximum LOD score of 3.84 was obtained 2.5 cM from the centromere with a support interval of 8 cM. Haplotype analysis of eight sons of Enhancer suggested that the UH gene is located in the centromeric end of BTA8 beyond ARO71/ARO72. Thus, by integrating the results from progeny of sire 3259 and sons of Enhancer the location of the UH gene was further refined to the BTA8 segment between ARO71/ARO72 and UWCA47.

Factors affecting incorrect paternity assignment in the Israeli Holstein population.

A total of 6040 Israeli Holstein cows from 181 Kibbutz herds listed as progeny of 11 sires were genotyped for 104 microsatellites. Seventeen markers were deleted due to a frequency of erroneous genotypes >1%, leaving 160,470 valid genotypes. Conflicts between the putative sire and daughter in at least 2 markers and for at least 10% of the markers genotyped per cow were required to reject paternity. Cows that did not meet the requirements for paternity confirmation or rejection were deleted from further analysis. The frequency of rejected paternity was 11.7%. The effects of recorded sire, birth year, geographical region, herd, and inseminator on the frequency of paternity rejection were analyzed with linear and nonlinear models. Only the effects of inseminator and recorded sire were significant in all models tested that included these effects. The main causes of incorrect paternity recording appear to be inseminator recording mistakes, and possibly mistakes with respect to semen labeling at the AI institutes. Incorrect paternity recording due to multiple inseminations by different sires could explain, at most, 20% of the paternity mistakes. Instituting a system of quality control, especially at the level of the inseminator, should reduce paternity errors to no more than 8%, and increase genetic progress by at least 1%.

A complete genome scan of the Israeli Holstein population for quantitative trait loci by a daughter design.

Eleven Israeli Holstein families including 5221 cows were analyzed by a daughter design for eight economic traits: milk, fat and protein production, fat and protein percentage, somatic cell score (SCS), herd-life, and female fertility. The cows were genotyped for 73 microsatellites with maximum spacing between markers of 53 cM. There were 86,304 informative genotypes. Preliminary analysis was by ANOVA of each trait, with the marker effect nested within sire. Significance was determined by controlling the false discovery rate at 0.4, after excluding markers with genome-wide significance for at least a single trait, and traits without any significant effects at this level. Thus, four markers on chromosomes 6 and 14 and female fertility were excluded. There remained 40 significant marker-trait combinations, and it is expected that 24 of these are true effects. To perform interval mapping for the families with significant contrasts, 21 additional markers were genotyped on chromosomes 2, 7, and 27. The bootstrap confidence intervals for gene effect did not include zero for protein percent on chromosome 2 and fat yield, protein yield, and SCS on chromosome 7. Quantitative trait locus heterozygosity was 33%, which is consistent with the hypothesis that only two alleles are segregating with unequal allele frequency.