International Mammalian Genome Society

The 16th International Mouse Genome Conference (2002)

Oral Presentation

Monday 18 November

22:00 - 22:15 HRS


F Iraqi

Co-Authors: 1) Naessens J, 2) Quackenbush J, 2) Gaspard R, 1) Nakamura Y, 1) Gibson J
Institutions: 1) International Livestock Research Institute (ILRI), 2) The Institute for Genomic Research (TIGR)

A/J mice, susceptible for Trypanosoma congolense, develop much higher parasitemia and die earlier than the more resistant  C57BL/6 mice.  It is believed that identification of the genes that contribute to resistance in this mouse model will lead to new control options for this disease. Intercrossing the two mouse strains and genotyping F2 mice representing the phenotypic extremes, as defined by time to death, allowed the identification of three major QTL regions, linked with resistance. Following the F2 results, the QTL were fine mapped using an F6 AIL population. As the genes responsible for this resistance should be linked with amplification or shut-down of particular metabolic pathways, a selection of differentially expressed genes may help in the identification of possible resistance genes, already restricted to the QTL regions. To that end, spleen and liver tissues from A/J and C57BL/6 mice were taken at different time points after infection with T. congolense.  For each time point and each tissue, RNA from 5 mice were pooled to minimise individual variation and subsequently used to hybridise with microarray consists ~27,000 mouse cDNAs representing ~22,000 unique genes.  To eliminate the environmental variations which can affect the infection, the whole experiment was conducted in duplicate.It has been shown that TNF-a plays a role in control of parasitemia in trypanosomosis. To help unravel the mechanism mediated by TNF-a, gene expression in TNF-a-deficient C57BL/6 mice was also compared to wild type mice. The results of the analysis will be presented at the meeting.

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