作者: Charles A. Day , Nicholas W. Baetz , Courtney A. Copeland , Lewis J. Kraft , Bing Han
DOI: 10.1111/TRA.12269
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摘要: How the plasma membrane is bent to accommodate clathrin-independent endocytosis remains uncertain. Recent studies suggest Shiga and cholera toxin induce curvature required for their uptake into carriers by binding cross-linking multiple copies of glycosphingolipid receptors on membrane. But it unclear if toxin-induced sphingolipid crosslinking provides sufficient mechanical force deforming membrane, or host cell factors also contribute this process. To test this, we imaged B-subunit surface-derived tubular invaginations. We found that mutants bind only one receptor accumulated in tubules, was entirely dispensable tubulations form. Unexpectedly, driving tubule extension supplied combination microtubules, dynein dynactin, thus defining a novel mechanism generating during endocytosis.