Based on the various findings presented here, we propose the following model for a role of caveolae and noncaveolar rafts in endocytosis (see also Ref. ). Non-caveolar lipid rafts, perhaps smaller than caveolae, fuse laterally and form pre-endocytic domains that may pinch off by both dynamin-dependent and -independent mechanisms. Such rafts may also become associated with caveolin. This association leads to a stable, defined curvature and size of the raft, and to a reduced ability to pinch off. The newly formed caveolae become associated with the actin cytoskeleton via filamin and are now immobilized. However, a small fraction of these caveolae may actually become constitutively internalized, perhaps as a means of caveolin turnover, either because they have not been sufficiently immobilized by the actin cytoskeleton and/or they contain too little caveolin. Molecules present in such caveolae may therefore become internalized. Moreover, cav-eolae may be involved in local, short-range motility, possibly including fission and fusion processes. Finally, in some cases - for example, after virus stimulation - a signaling cascade may be initiated, leading to reorganization of the actin cytoskeleton and recruitment of dynamin, and a subsequent wave of internalized caveolae, which are only very slowly replaced. Considering all the other functions ascribed to caveolin/caveolae at the plasma membrane (see Section 4.1), such a massive, long-lasting down-regulation of caveolae can, however, hardly be considered a physiologically desirable situation for the cell.
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