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Human Molecular Genetics, Vol 7, 743-750, Copyright © 1998 by Oxford University Press

ARTICLES

Characterization of lpd (lipid defect): a novel mutation on mouse chromosome 16 associated with a defect in triglyceride metabolism

XY Wen, DM Bryce and ML Breitman
Division of Molecular and Developmental Biology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada. x.wen@utoronto.ca

Recent epidemiological studies have identified plasma triglyceride as a risk factor for atherogenesis. We have generated a mouse transgenic line that carries a recessive mutation designated lpd (lipid defect). Homozygous lpd mice develop as runts and die by age 10-15 days with striking liver pathology characterized by the presence of numerous lipid-containing vacuoles and extensive accumulation of triglycerides. Cloning of the mutant insertion locus and the wild-type lpd locus have revealed a duplication of host genomic sequences at the site of integration. Mapping of the lpd locus with the Jackson Laboratory BSS interspecific backcross panel of (C57BL/6JEi x SPRET/Ei) F1 x SPRET/Ei placed the lpd locus to the distal part of chromosome 16. These observations suggest that the transgene disrupts a putative gene at the lpd locus and that lpd is a novel locus related to triglyceride metabolism. The lpd mutant mice may serve as models for human disorders of fatty livers or hypertriglyceridemia.
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