Journal of Lipid Research, Vol 31, 955-963, Copyright © 1990 by Lipid Research, Inc.

ARTICLES

Spontaneous high density lipoprotein deficiency syndrome associated with a Z-linked mutation in chickens

F Poernama, SA Schreyer, JJ Bitgood, ME Cook and AD Attie
Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin, Madison 53706.

A mutant strain of chicken previously identified by a "recessive white skin" phenotype was found to have a profound deficiency in high density lipoprotein (HDL) and apolipoprotein A-I (apoA-I). ApoA-I levels in the mutant chickens were reduced by greater than 90%. Since HDL is the predominant cholesterol transporter in chickens, the HDL deficiency was associated with a greater than 80% decrease in total plasma cholesterol. The mutation segregates with markers linked to the Z- chromosome. The structure of the apoA-I produced by the mutant chickens appeared normal as judged by two-dimensional gel electrophoresis. The genetic and biochemical evidence, therefore, suggests that the mutation is not in the apoA-I structural gene. Turnover studies were performed on labeled HDL or on labeled apoA-I preincubated with HDL prior to intravenous injection. Both types of experiments showed that both defective apoA-I production and hypercatabolism contributed to the HDL deficiency, although defective production made a much larger contribution.
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