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Originally published as Genetics Published Articles Ahead of Print on December 30, 2005.
Genetics, Vol. 172, 1799-1807, March 2006, Copyright © 2006
doi:10.1534/genetics.105.051912
Quantitative Trait Locus Analysis of Atherosclerosis in an Intercross Between C57BL/6 and C3H Mice Carrying the Mutant Apolipoprotein E Gene
Zhiguang Su*,
,
Yuhua Li*,,
Jessica C. James*,,
Marcia McDuffie
,
Alan H. Matsumoto*,
Gregory A. Helm
,
James L. Weber**,
Aldons J. Lusis and
Weibin Shi*,,1
* Department of Radiology, Department of Neurosurgery, and Department of Microbiology, and the Cardiovascular Research Center, University of Virginia, Charlottesville, Virginia 22908, ** Center for Medical Genetics, Marshfield Medical Research Foundation, Marshfield, Wisconsin 54449 and Departments of Medicine and Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, California 90095-1679
1 Correspondence: University of Virginia, Department of Radiology, Box 801339, Room 1171, MR4, 409 Lane Rd., Charlottesville, VA 22908.
E-mail: ws4v{at}virginia.edu
Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) differ significantly in atherosclerosis susceptibility and plasma lipid levels on the apolipoprotein E-deficient (apoE–/–) background when fed a Western diet. To determine genetic factors contributing to the variations in these phenotypes, we performed quantitative trait locus (QTL) analysis using an intercross between the two strains carrying the apoE–/– gene. Atherosclerotic lesions at the aortic root and plasma lipid levels of 234 female F2 mice were analyzed after being fed a Western diet for 12 weeks. QTL analysis revealed one significant QTL, named Ath22 (42 cM, LOD 4.1), on chromosome 9 and a suggestive QTL near D11mit236 (20 cM, LOD 2.4) on chromosome 11 that influenced atherosclerotic lesion size. One significant QTL on distal chromosome 1, which accounted for major variations in plasma LDL/VLDL cholesterol and triglyceride levels, coincided with a QTL having strong effects on body weight. Plasma LDL/VLDL cholesterol or triglyceride levels of F2 mice were significantly correlated with body weight, but they were not correlated with atherosclerotic lesion sizes. These data indicate that atherosclerosis susceptibility and plasma cholesterol levels are controlled by separate genetic factors in the B6 and C3H mouse model and that genetic linkages exist between body weight and lipoprotein metabolism.
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