International Mammalian Genome Society

The 16th International Mouse Genome Conference (2002)


POSTER 114 - QTL FINE MAPPING AND MICROARRAY ANALYSIS TO ELUCIDATE THE MOLECULAR BASIS OF OBESITY IN LINES OF MICE DIVERGENTLY SELECTED ON FAT CONTENT

I M Stylianou
Roslin Institute & Institute of Cell, Animal and Population Biology, University of Edinburgh

1&2) Stylianou I M, 2) Keightley P D, 2&3) BŁnger L, 1) Clinton M, 1) Bulfield G, 4) Pritchard C, 4) Underhill P, 4)Tymowska-Lalanne Z, 1&5) Horvat S.
1) Roslin Institute, 2) Institute of Cell, Animal and Population Biology, University of Edinburgh, 3) Animal Breeding & Genetics Dept, Animal Biology Division, SAC, 4) Harwell Microarray Facility, Medical Research Council, 5) University of Ljubljana, Biotechnical Faculty, Zootechnical Department

Obesity is proving to be a serious health concern in the developed world. Advances in genetics have brought to light a number of monogenic causes of obesity, however these have been shown to be responsible for only a few human cases of obesity. As a model of polygenic obesity, divergent selection for high and low fat content has been carried out for over 60 generations creating fat (F) and lean (L) -lines of mice resembling the nature of obesity observed in the human population. From crosses of these lines, four body fat quantitative trait loci (QTL) were identified (Horvat et al. 2000, Mamm Genome. 11(1): 2-7). We have since created a congenic line (Fchr15L), by repeated backcrossing to introgress the QTL with the largest effect on chromosome 15 (Fob3) from the L-line into the F-line background. We have shown the interval of Fob3 to be about 16cM accounting for a difference in body fat of 25%. Here we report on further fine mapping of Fob3, by progeny testing of F2 recombinants produced from crosses between F-line and congenic Fchr15L mice. In addition, microarray analysis has identified known and anonymous transcripts that are differentially expressed between the F-line and Fchr15L-line. This may ultimately lead to the identification of the causal polymorphism(s) responsible for the QTL effect and identify altered pathways differing between the lines. Such knowledge may prove useful towards the development of treatments for human obesity or in the farming industry wishing to produce leaner meat.


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