|MARSHALL, KAREN - International Livestock Research Institute (ILRI) - Kenya|
|NAGDA, SONAL - International Livestock Research Institute (ILRI) - Kenya|
|GIBSON, JOHN - University Of New England|
|HANOTTE, OLIVIER - University Of Nottingham|
|SILVA, MARCOS - Embrapa|
|BAKER, L. - Collaborator|
|Van Tassell, Curtis - Curt|
Submitted to: Animal Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/3/2012
Publication Date: 6/15/2013
Citation: Marshall, K., Nagda, S., Gibson, J.P., Sonstegard, T.S., Hanotte, O., Silva, M.V., Baker, L., Van Tassell, C.P. 2013. Quantitative trait loci for resistance to Haemonchus contortus under artificial challenge in Red Maasai and Dorper sheep of East Africa. Animal Genetics. 44(3):285-295.
Interpretive Summary: This report is a continuation of a previous study to try to identify genomic regions or genes affecting host genetic response of sheep to parasitic infection. In the first study, the regions were mapped based on parasite indicator traits recorded from natural exposure to parasites on pasture. This study uses the same DNA marker data generated from the previous field study and contrasts them to the second set of phenotypic data recorded from artificial or experimental challenges of the sheep to parasites. The main regions found in this study differed from the previous study, and strongly suggest a region on Chr 26 involved in a number of immune response parameters for host tolerance to parasites.
Technical Abstract: A genome-wide scan was performed to detect quantitative trait loci (QTL) for resistance to the gastro-intestinal 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 measured including fecal egg count, packed cell volume decline, and abomasal worm counts. A subset of the population (342 lambs) were selectively genotyped for 172 microsatellite loci covering 25 of the 26 autosomes. QTL mapping was performed for models that assumed the QTL alleles were either fixed or unfixed segregating within a breed, combined with models that fitted an additive QTL effect only or both an additive and dominant dominance QTL effects. Overall, QTL significant at the 1% chromosome-wide level were identified for 22 traits by chromosome combinations. Of particular interest was a region on chromosome 26 that had putative QTL for all nine traits, and a region on chromosome 2 that had putative QTL for three traits. Favorable QTL alleles for disease resistance were a mixture of Red Maasai and Dorper origin, were not always fixed within breed, and in some cases had significant dominance effects. We anticipate that this study, in combination with follow-up work and other studies, will help elucidate the biology of disease resistance.