作者: Takahiro K. Fujiwara , Kokoro Iwasawa , Ziya Kalay , Taka A. Tsunoyama , Yusuke Watanabe
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摘要: The mechanisms by which the diffusion rate in plasma membrane (PM) is regulated remain unresolved, despite their importance spatially regulating reaction rates PM. Proposed models include entrapment nanoscale noncontiguous domains found PtK2 cells, slow due to crowding, and actin-induced compartmentalization. Here, applying single-particle tracking at high time resolutions, mainly PtK2-cell PM, we confined plus hop movements (termed "hop diffusion") for both a nonraft phospholipid transmembrane protein, transferrin receptor, equal compartment sizes these two molecules all five of cell lines used here (actual were dependent), even after treatment with actin-modulating drugs. cross-section size cytoplasmic domain affected frequency. Electron tomography identified actin-based skeleton (MSK) located within 8.8 nm from PM surface cells demonstrated that MSK mesh was same as molecular diffusion. extracellular matrix proteins not involved These results support model anchored TM-protein pickets lining major mechanism