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J. Biol. Chem., Vol. 275, Issue 21, 15609-15612, May 26, 2000
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From the The terminal step in triglyceride
biosynthesis is the esterification of diacylglycerol. To study this
reaction in the model eukaryote, Saccharomyces cerevisiae,
we investigated five candidate genes with sequence conservation to
mammalian acyltransferases. Four of these genes are similar to the
recently identified acyl-CoA diacylglycerol acyltransferase and, when
deleted, resulted in little or no decrease in triglyceride synthesis as
measured by incorporation of radiolabeled oleate or glycerol. By
contrast, deletion of LRO1, a homolog of human lecithin
cholesterol acyltransferase, resulted in a dramatic reduction in
triglyceride synthesis, whereas overexpression of LRO1
yielded a significant increase in triglyceride production. In
vitro microsomal assays determined that Lro1 mediated the
esterification of diacylglycerol using phosphatidylcholine as the acyl
donor. The residual triglyceride biosynthesis that persists in the
LRO1 deletion strain is mainly
acyl-CoA-dependent and mediated by a gene that is
structurally distinct from the previously identified mammalian
diacylglycerol acyltransferase. These mechanisms may also exist in
mammalian cells.
ACCELERATED PUBLICATION
A Lecithin Cholesterol Acyltransferase-like Gene Mediates
Diacylglycerol Esterification in Yeast*
,,
,, and**
Institute of Human Nutrition and the
** Departments of Pediatrics, Physiology, and Cellular Biophysics, and
§ Genetics and Development, Columbia University College
of Physicians and Surgeons, New York, New York 10032 and the
DuPont Pharmaceutical Company, Experimental Station, Wilmington,
Delaware 19880-0400
*
This work was supported in part by the Hirschl/Weil-Caulier
Trust and the Ara Parseghian Medical Research Foundation (to
S. L. S.). P. O. and A. T. were supported by National Institutes of
Health postdoctoral training fellowships in Atherosclerosis (HL07343
from NHLBI) and Nutrition (DK07715 from NIDDK), respectively.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.
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.
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