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Summary A genome-wide scan for quantitative trait loci (QTL) affecting gastrointestinal nematode resistance in sheep was completed using a double backcross population derived from Red Maasai and Dorper ewes bred to F1 rams. This design provided an opportunity to map potentially unique genetic variation associated with a parasite-tolerant breed like Red Maasai, a breed developed to survive East African grazing conditions. Parasite indicator phenotypes (blood packed cell volume – PCV and faecal egg count – FEC) were collected on a weekly basis from 1064 lambs during a single 3-month post-weaning grazing challenge on infected pastures. The averages of last measurements for FEC (AVFEC) and PCV (AVPCV), along with decline in PCV from challenge start to end (PCVD), were used to select lambs (N = 371) for genotyping that represented the tails (10% threshold) of the phenotypic distributions. Marker genotypes for 172 microsatellite loci covering 25 of 26 autosomes (1560.7 cm) were scored and corrected by Genoprob prior to qxpak analysis that included Box–Cox transformed AVFEC and arcsine transformed PCV statistics. Significant QTL for AVFEC and AVPCV were detected on four chromosomes, and this included a novel AVFEC QTL on chromosome 6 that would have remained undetected without Box–Cox transformation methods. The most significant P-values for AVFEC, AVPCV and PCVD overlapped the same marker interval on chromosome 22, suggesting the potential for a single causative mutation, which remains unknown. In all cases, the favourable QTL allele was always contributed from Red Maasai, providing support for the idea that future marker-assisted selection for genetic improvement of production in East Africa will rely on markers in linkage disequilibrium with these QTL.

The introduction of web based mapping facilities that use satellite imagery, offers local people the possibility to map their environment. However, maps need to be accurate, which is the reason why map making is assigned to professionals. In this paper, we investigated the classification accuracy of road infrastructure from high resolution satellite imagery of an urban area in western Kenya achieved by surveyors and non-surveyors alike, with and without local knowledge. Those with local knowledge classified roads with over 92% accuracy on average, irrespective of surveying background. Professional surveyors and laymen without local knowledge achieved lower accuracies of 67.7% and 42.9% respectively. We argue that local knowledge is also likely to improve the classification accuracy of many other attributes featured in topographic maps and thus conclude that there is reason to consider engaging local expertise in the production and updating of topographic maps.

Summary Microsatellite markers are commonly used for population genetic analyses of livestock. However, up to now, combinations of microsatellite data sets or comparison of population genetic parameters from different studies and breeds has proven difficult. Often different genotyping methods have been employed, preventing standardization of microsatellite allele calling. In other cases different sets of markers have been genotyped, providing differing estimates of population genetic parameters. Here, we address these issues and illustrate a general two-step regression approach in cattle using three different sets of microsatellite data, to combine population genetics estimates of diversity and admixture. This regression-based method is independent of the loci genotyped but requires common breeds in the data sets. We show that combining microsatellite data sets can provide new insights on the origin and geographical distribution of genetic diversity and admixture in cattle, which will facilitate global management of this livestock species.

Susceptible A/J and more resistant C57BL/6J mice were infected with Plasmodium chabaudi chabaudi 54X, P.c. chabaudi AS and Plasmodium chabaudi adami 408XZ. As expected, most C57BL/6J mice survived the infections with the different isolates. But in contrast to previous observations, not all A/J mice succumbed to infection: just over 50% of A/J mice survived infections with P.c. chabaudi 54X, while 80% survived P.c. chabaudi AS. The more virulent parasite, P.c. adami 408XZ, was able to kill all A/J mice and 20% of C57BL/6J mice after an intravenous infection with 105 pRBC. A detailed study of four parameters of pathology (body weight, body temperature, blood glucose and RBC counts) in both mouse strains after a P.c. adami 408XZ infection showed similar patterns to those previously reported after infection with P.c. chabaudi AS. These data suggest that environmental factors as well as parasite polymorphisms might influence the severity of malaria between susceptible and resistant mice.

We developed an F(11) AIL population from an F(1) cross of A/J (susceptible) and C57BL/6J (resistant) mouse strains. One thousand F(11) mice were challenged with P.c. chabaudi 54X, and 340 mice selected from the phenotypic extremes for susceptibility and resistance were genotyped for microsatellite markers on Chromosomes (Chrs) 5, 8, and 17. QTL originally detected in backcross and F(2) populations were confirmed on the three chromosomes within narrower genomic regions, by maximum likelihood and regression analyses. Each of the previously mapped QTL on Chrs 5 and 17 resolved into two linked QTLs. The distal and proximal QTLs on Chrs 5 and 17, respectively, map to the previously reported QTL.

Summary A genome-wide scan was performed to detect quantitative trait loci (QTL) for resistance to the gastrointestinal nematode Haemonchus contortus in a double backcross population of Red Maasai and Dorper sheep. The mapping population comprised six sire families, with 1026 lambs in total. The lambs were artificially challenged with H. contortus at about 6.5 months of age, and nine phenotypes were measured: fecal egg count, packed cell volume decline, two weight traits and five worm traits. A subset of the population (342 lambs) was selectively genotyped for 172 microsatellite loci covering 25 of the 26 autosomes. QTL mapping was performed for models which assumed that the QTL alleles were either fixed or segregating within each breed, combined with models with only an additive QTL effect fitted or both additive and dominance QTL effects fitted. Overall, QTL significant at the 1% chromosome-wide level were identified for 22 combinations of trait and chromosome. Of particular interest are a region of chromosome 26 with putative QTL for all nine traits and a region of chromosome 2 with putative QTL for three traits. Favorable QTL alleles for disease resistance originated in both the Red Maasai and Dorper breeds, were not always fixed within breed and had significant dominance effects in some cases. We anticipate that this study, in combination with follow-up work and other relevant studies, will help elucidate the biology of disease resistance.

SUMMARYA comparison of F2 and F6/7 inter-cross lines of mice, derived from CBA and SWR parental strains, has provided strong evidence for several previously undetected quantitative trait loci (QTL) for resistance to Heligmosomoides bakeri. Five QTL affecting average faecal egg counts and/or worm burdens in week 6 were detected on mouse chromosomes 5 (Hbnr9 and Hbnr10), 8 (Hbnr11) and 11 (Hbnr13 and Hbnr14). Three QTL for faecal egg counts in weeks 4 and 6 were found on both chromosomes 5 (Hbnr9) and 11 (Hbnr13 and Hbnr14). Two QTL for the mucosal mast cell protease 1 (MCPT1) response were located on chromosomes 8 (Hbnr11) and 11 (Hbnr13), two for the IgG1 antibody response to adult worms on chromosomes 5 (Hbnr10) and 8 (Hbnr11), two for PCV in week 6 on chromosomes 5 (Hbnr9) and 11 (Hbnr13), and two for the granulomatous response on chromosome 8 (Hbnr12) and 11 (Hbnr15). Our data emphasize that the control of resistance to H. bakeri is multigenic, and regulated by genes within QTL regions that have a complex range of hierarchical relationships.

Fine mapping of quantitative trait loci (QTL) associated with resistance to the gastrointestinal parasite Heligmosomoides polygyrus was achieved on F(6)/F(7) offspring (1076 mice) from resistant (SWR) and susceptible (CBA) mouse strains by selective genotyping (top and bottom 20% selected on total worm count in week 6). Fecal egg counts were recorded at weeks 2, 4, and 6, and the average was also analyzed. Blood packed cell volume in weeks 3 and 6 and five immunological traits (mucosal mast cell protease 1, granuloma score, IgG1 against adult worm, IgG1, and IgE to L4 antigen) were also recorded. On Chromosome 1 single-trait analyses identified a QTL with effects on eight traits located at about 24 cM on the F(2) mouse genome database (MGD) linkage map, with a 95% confidence interval (CI) of 20-32 cM established from a multitrait analysis. On Chromosome 17 a QTL with effects on nine traits was located at about 18 cM on the MGD map (CI 17.9-18.4 cM). Strong candidate genes for the QTL position on Chromosome 1 include genes known to be involved in regulating immune responses and on Chromosome 17 genes within the MHC, notably the Class II molecules and tumor necrosis factor.