J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on November 1, 2004

Papers In Press, published online ahead of print August 16, 2004
J. Lipid Res., doi:10.1194/jlr.M400136-JLR200
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Submitted on April 8, 2004
Revised on July 30, 2004
Accepted on August 2, 2004

Epistatic interaction between two non-structural Loci on chromosomes 7 and 3 influences hepatic lipase activity in BSB mice

Nengjun Yi, Sally Chiu, David B. Allison, Janis S. Fisler, and Craig H. Warden

Department of Pediatrics, University of California at Davis, Davis, CA 95616

Corresponding Author: chwarden{at}ucdavis.edu

BSB mice exhibit a wide range of obesity despite being produced by a backcross of lean C57BL/6J (B) x lean Mus spretus (SPRET/Pt) F1s x B. Previous linkage studies identified a quantitative trait locus (QTL) on mouse chromosome 7 with co-incident peaks for hepatic lipase activity, obesity and plasma cholesterol. However, these mice were not analyzed for gene x gene epistasis. Hepatic lipase activity is correlated with obesity and plasma cholesterol levels. In this study, we identified QTL for plasma hepatic lipase activity with three statistical mapping methods: maximum likelihood interval mapping, Bayesian non-epistatic mapping, and Bayesian epistatic mapping. Bayesian epistatic mapping detected not only the QTL on chromosome 7, but also an additional QTL on chromosome 3, which has a weak main effect but a strong interaction with chromosome 7. SPRET/Pt alleles of the QTL on each chromosome promote hepatic lipase activity. The proportion of phenotypic variance explained by the epistatic effect is higher than that explained by the main effect of QTL on chromosome 7.


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 GeneticsHome page
N. Yi, B. S. Yandell, G. A. Churchill, D. B. Allison, E. J. Eisen, and D. Pomp
Bayesian Model Selection for Genome-Wide Epistatic Quantitative Trait Loci Analysis
Genetics, July 1, 2005; 170(3): 1333 - 1344.
[Abstract] [Full Text] [PDF]


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