International Mammalian Genome Society

The 16th International Mouse Genome Conference (2002)


D Menge
Jomo Kenyatta University of Agriculture and Technology

1) Menge D, 2)Behnke J, 2) Lowe A, 4) Gibson J, 3) Baker L, 2) Wakelin D, 3) Iraqi A F
1) University Tennessee Health Science Center, 2) Oak Ridge National Laboratory, 3) University of Tennessee, Knoxville, 4) University of Memphis, 5) University of Washington

Gastro-intestinal nematodes are arguably the most important disease which restricts the production of domestic ruminants in developing and developed countries. Current control mainly relies on chemotherapy, but resistance to major anthelmintics is widely reported. An alternative approach for controlling the disease is to breed ruminants with enhanced resistance to the infection. There is  considerable effort to understand the  mechanisms  controlling the disease in sheep and in mouse models. Here we report results of a genome-wide search for QTL influencing immunological responses to the disease in an F2 cross of resistant SWR and susceptible CBA parents, following  trickle infection with Heligmosomoides polygyrus. Sera was collected at week 6 of infection and assayed by ELISA for mucosal mast cell proteases and antibodies against adult worm antigen for parasite specific IgG1 and IgE titers. Granuloma score on the intestinal mucosa was recorded  post-mortem. The susceptible CBA mice had significantly higher IgG1, but significantly lower IgE, granuloma and mucosal mast cell proteases than SWR mice. Significant QTL were mapped to chromosomes 4, 11, 13 and 17 for granuloma; chromosomes 12 and 17 for IgE; chromosome 10, 17 and 18 for IgG1 and chromosomes 1, 9, 11, 17 and 18 for mucosal mast cell proteases. Multiple QTL were detected on chromosomes 11 and 17 in about the same position and with consistently negative or positive effects indicating a pleiotropic mechanism.  QTL on other chromosomes were distinct. Fine mapping of these QTL is ongoing using the advanced intercross line (AIL) approach.

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