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J. Biol. Chem., Vol. 262, Issue 16, 7594-7604, Jun, 1987
AJ Lusis, BA Taylor, D Quon, S Zollman and RC LeBoeuf
We report the identification and partial characterization of polymorphisms
among inbred strains of mice affecting several aspects of the expression of
apolipoproteins B and E (apoB and apoE), the major proteins of low density
lipoproteins (LDL) and very low density lipoproteins (VLDL). These
polymorphisms include differences in the levels of the lipoproteins and
apolipoproteins on both chow and high fat diets, differences in their
response to a high fat diet challenge, and differences in the relative
levels of the two molecular weight species of apoB. Although most strains
exhibited a large increase in plasma LDL and VLDL in response to a high fat
diet, the levels of apoB and apoE mRNA were either unaffected or, in some
cases, decreased slightly. Also, the levels of apoB and apoE mRNA were not
correlated among strains with the levels of the apolipoproteins in plasma,
suggesting that genetic control occurs primarily at the level of
lipoprotein catabolism. Elucidation of the precise mechanisms involved in
the differences will require genetic analysis. Toward this end, we have
identified DNA polymorphisms for apoB and apoE and have used these in
segregation analysis to determine the chromosomal locations of the apoB and
apoE structural genes in mice. The gene for apoB, designated Apob, resides
in the proximal region of chromosome 12 linked to genes for ribosomal RNA
and aryl hydrocarbon hydroxylase. The gene for apoE, designated Apoe, is
located on chromosome 7, linked to genes for glucose phosphate isomerase
and peptidase 4. Previously, we mapped the structural genes for
apolipoproteins A-I and A-II to mouse chromosomes 9 and 1, respectively,
and thus, the four loci encoding mammalian apolipoproteins have now been
located in the mouse. These loci are homologous to the loci encoding
apolipoproteins in humans as judged by the conservation of linked markers.
A correlation was observed between a unique apoB allele and
"responsiveness" to a high fat diet challenge. There were no obvious
associations of apoB, apoE, or LDL/VLDL phenotypes or genotypes with
diet-induced atherosclerosis among strains surveyed. These results clarify
the organization and regulation of the genes for apoB and apoE, and they
provide information about the naturally occurring polymorphisms affecting
their expression.
Genetic factors controlling structure and expression of apolipoproteins B and E in mice
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