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Originally published In Press as doi:10.1074/jbc.C000710200 on November 3, 2000

J. Biol. Chem., Vol. 275, Issue 52, 40667-40670, December 29, 2000
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ACCELERATED PUBLICATION
Mutations in Yeast ARV1 Alter Intracellular Sterol Distribution and Are Complemented by Human ARV1*

Arthur H. TinkelenbergDagger , Ying LiuDagger , Frederick AlcantaraDagger , Sohail KhanDagger , Zhongmin GuoDagger , Martin Bard§, and Stephen L. SturleyDagger ||**

From the Dagger  Institute of Human Nutrition and Departments of  Pediatrics and || Physiology and Cellular Biophysics, Columbia University College of Physicians and Surgeons, New York, New York 10032 and the § Department of Biology, Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202

Intracellular cholesterol redistribution between membranes and its subsequent esterification are critical aspects of lipid homeostasis that prevent free sterol toxicity. To identify genes that mediate sterol trafficking, we screened for yeast mutants that were inviable in the absence of sterol esterification. Mutations in the novel gene, ARV1, render cells dependent on sterol esterification for growth, nystatin-sensitive, temperature-sensitive, and anaerobically inviable. Cells lacking Arv1p display altered intracellular sterol distribution and are defective in sterol uptake, consistent with a role for Arv1p in trafficking sterol into the plasma membrane. Human ARV1, a predicted sequence ortholog of yeast ARV1, complements the defects associated with deletion of the yeast gene. The genes are predicted to encode transmembrane proteins with potential zinc-binding motifs. We propose that ARV1 is a novel mediator of eukaryotic sterol homeostasis.

* This work was supported by the Ara Parseghian Medical Research Foundation, the Hirschl/Weil-Caulier Trust, and by the National Institutes of Health (Grant DK54320 to S. L. S., Grant GM62104 to M. B., and Postdoctoral Training Fellowship DK07715 in nutrition to A. H. T.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF290878.

** Established Investigator of the American Heart Association. To whom correspondence should be addressed: Inst. of Human Nutrition, Columbia University College of Physicians and Surgeons, 650 W. 168th St., New York, NY 10032. Tel.: 212-305-6304; Fax: 212-305-3079; E-mail: sls37@columbia.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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