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SDPR induces membrane curvature and functions in the formation of caveolae
Caveolae are plasma membrane invaginations with a characteristic flask shaped morphology. They function in diverse cellular processes, including endocytosis. The mechanism by which caveolae are generated is not fully understood, but both caveolin proteins and Polymerase I and Transcript Release Fact...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712677/ https://www.ncbi.nlm.nih.gov/pubmed/19525939 http://dx.doi.org/10.1038/ncb1887 |
Sumario: | Caveolae are plasma membrane invaginations with a characteristic flask shaped morphology. They function in diverse cellular processes, including endocytosis. The mechanism by which caveolae are generated is not fully understood, but both caveolin proteins and Polymerase I and Transcript Release Factor (PTRF, also called cavin) are important. Here we show that loss of SDPR, a caveolar protein homologous to PTRF, causes loss of caveolae. SDPR binds directly to PTRF and recruits PTRF to caveolar membranes. Over-expression of SDPR, unlike PTRF, induces deformation of caveolae and extensive tubulation of the plasma membrane. The B-subunit of shiga toxin (STB) also induces membrane tubulation, and these membrane tubes also originate from caveolae. STB co-localizes extensively with both SDPR and caveolin 1. Loss of caveolae reduces the propensity of STB to induce membrane tubulation. We conclude that SDPR is a membrane-curvature inducing component of caveolae, and that STB-induced membrane tubulation is facilitated by caveolae. |
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