Increase in membrane cholesterol: A possible trigger for degradation of HMG CoA reductase and crystalloid endoplasmic reticulum in UT-1 cells |
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Authors: | Lelio Orci Michael S. Brown Joseph L. Goldstein Luis M. Garcia-Segura Richard G.W. Anderson |
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Affiliation: | 1. Institute of Histology and Embryology University of Geneva Medical School Geneva, Switzerland;2. Department of Molecular Genetics University of Texas Health Science Center Southwestern Medical School Dallas, Texas 75235 USA;3. Department of Cell Biology University of Texas Health Science Center Southwestern Medical School Dallas, Texas 75235 USA |
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Abstract: | The crystalloid endoplasmic reticulum (ER) houses large amounts of HMG CoA reductase, the rate-controlling enzyme in cholesterol synthesis. The crystalloid ER appears in UT-1 cells, a line of Chinese hamster ovary cells that has been chronically starved of cholesterol as a result of growth in the presence of compactin, an inhibitor of reductase. When cholesterol was provided to UT-1 cells in the form of low density lipoprotein (LDL), the reductase and crystalloid ER were destroyed. This destruction was preceded by an increase in the cholesterol content of crystalloid ER membranes, as judged by a 4- to 8-fold increase in their ability to form complexes with filipin, a cholesterol-binding compound that can be visualized in freeze-fracture electron micrographs. Filipin binding to other membranes was unchanged. Thus insertion of cholesterol into the crystalloid ER membrane may trigger the degradation of reductase and the membrane itself. |
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