Trypanosomosis, or sleeping sickness, is a major disease constraint on livestock productivity in sub-Saharan Africa. To identify quantitative trait loci (QTL) controlling resistance to trypanosomosis in cattle, an experimental cross was made between trypanotolerant African N'Dama (Bos taurus) and trypanosusceptible improved Kenya Boran (Bos indicus) cattle. Sixteen phenotypic traits were defined describing anemia, body weight, and parasitemia. One hundred seventy-seven F2 animals and their parents and grandparents were genotyped at 477 molecular marker loci covering all 29 cattle autosomes. Total genome coverage was 82%. Putative QTL were mapped to 18 autosomes at a genomewise false discovery rate of <0.20. The results are consistent with a single QTL on 17 chromosomes and two QTL on BTA16. Individual QTL effects ranged from Ϸ6% to 20% of the phenotypic variance of the trait. Excluding chromosomes with ambiguous or nontrypanotolerance effects, the allele for resistance to trypanosomosis originated from the N'Dama parent at nine QTL and from the Kenya Boran at five QTL, and at four QTL there is evidence of an overdominant mode of inheritance. These results suggest that selection for trypanotolerance within an F2 cross between N'Dama and Boran cattle could produce a synthetic breed with higher trypanotolerance levels than currently exist in the parental breeds.

Mutations of the connexin 26 gene (GJB2) were studied in 365 apparently unrelated individuals with profound nonsyndromic, sensorineural hearing impairment from Ghana, West Africa. Among 121 mutated chromosomes found, 110 carried the previously described R143W mutation. A total of 6 novel mutations: L79P, V178A, R184Q, A197S, I203K, and L214P, were identified, whereby I203K was based on a dinucleotide exchange and R184Q appeared to be dominant. The GJB2 variants found in Ghana tend to comprise less nonsense and frameshift mutations and more mutations located in the C-terminal half of the molecule than the variants found in other parts of the world.