Knockout of cav-1 protein causes loss of a cellular organelle

Scientists from the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, the Franz Volhard Clinic of the Charit, Humboldt-University Berlin and Max Delbrck Center for Molecular Medicine, Berlin-Buch, were able to cause loss of caveolae and by studying mice lacking this organelle, describe the function of caveolae in mammals. The latest issue of the scientific journal "Science" (published online August 9, 2001; 10.1126/science. 1062688 (Science Express Reports)) reports the current status of the research "Loss of caveolae, vascular dysfunction and pulmonary defects in caveolin-1 gene-disrupted mice".

An exciting new discovery and possibly providing the first example of an organelle knockout is the absence of caveolae after the protein caveolin-1 (cav-1) is genetically prevented from being expressed in transgenic mice. The scientists have characterised the phenotype of transgenic mice that lack caveolin-1 and have found that the mice lack caveolae, the small cave-like invaginations of the plasma membrane of a variety of eukaryotic cells. More than 50 years after the discovery of caveolae their function remains a matter of speculation and controversy. The study provides clues as to the function of these organelles and also provides the first example of the effect of removing a cellular organelle.

Caveolae have been associated with various cellular processes such as transcytosis of solutes through endothelial cells, cholesterol transport, signal transduction and tumor suppression. They have a characteristic flask-shape with a diameter of 50-100 nm and are present on many cell types, including endothelial, smooth muscle cells and fat cells. They represent a form of lipid rafts within the plasma membrane, enriched in cholesterol and glycolipids. Cav-1, a small protein of only 21-22 kDa, is to date the best biochemical marker for caveolae. It is assumed to be the major structural component of the caveolar coat that is seen in electron mi

Contact: Claudia Lorenz

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