The targeted Pon3 gene encodes a glycoprotein enzyme that interacts with high density lipoprotein (HDL) and hydrolyzes lactones. These mice carry a knock-out allele of Pon3 in which exon 4 has been replaced by a NEO cassette. No gene product (mRNA or protein) is detected by qPCR or Western blot analysis of liver from homozygotes. No lovastatinase activity is detected in liver homogenates from homozygous mice. When fed a cholate-cholesterol diet (15.8% fat, 1.25% cholesterol, and 0.5% sodium cholate), female knock-out mice develop larger (60% increase) atherosclerotic lesion size; 65% survival; increased levels of plasma total cholesterol, cholesterol ester, unesterified cholesterol; and decreased liver triglyceride levels compared to wildtype controls.
Mice that are homozygous for the targeted mutation are viable and fertile.
During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background.

This Pon3 knock-out strain exhibits altered liver lipid levels and increased mortality on a cholate-cholesterol diet. These mice may be suitable for use in studies of atherosclerosis and obesity.

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