网格蛋白轻链是回转网格蛋白回收途径所必需的，从而促进细胞迁移。
Clathrin light chains are required for the gyrating-clathrin recycling pathway and thereby promote cell migration.
作者信息
Majeed Sophia R, Vasudevan Lavanya, Chen Chih-Ying, Luo Yi, Torres Jorge A, Evans Timothy M, Sharkey Andrew, Foraker Amy B, Wong Nicole M L, Esk Christopher, Freeman Theresa A, Moffett Ashley, Keen James H, Brodsky Frances M
机构信息
1] Department of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, California 94143, USA [2] Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94143, USA [3] Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143, USA [4] The G.W. Hooper Foundation, University of California San Francisco, San Francisco, California 94143, USA.
1] Department of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, California 94143, USA [2] Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94143, USA [3] Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California 94143, USA [4] The G.W. Hooper Foundation, University of California San Francisco, San Francisco, California 94143, USA [5].
出版信息
Nat Commun. 2014 May 23;5:3891. doi: 10.1038/ncomms4891.
The clathrin light chain (CLC) subunits participate in several membrane traffic pathways involving both clathrin and actin, through binding the actin-organizing huntingtin-interacting proteins (Hip). However, CLCs are dispensable for clathrin-mediated endocytosis of many cargoes. Here we observe that CLC depletion affects cell migration through Hip binding and reduces surface expression of β1-integrin by interference with recycling following normal endocytosis of inactive β1-integrin. CLC depletion and expression of a modified CLC also inhibit the appearance of gyrating (G)-clathrin structures, known mediators of rapid recycling of transferrin receptor from endosomes. Expression of the modified CLC reduces β1-integrin and transferrin receptor recycling, as well as cell migration, implicating G-clathrin in these processes. Supporting a physiological role for CLC in migration, the CLCb isoform of CLC is upregulated in migratory human trophoblast cells during uterine invasion. Together, these studies establish CLCs as mediating clathrin-actin interactions needed for recycling by G-clathrin during migration.
网格蛋白轻链（CLC）亚基通过与肌动蛋白组织相关的亨廷顿相互作用蛋白（Hip）结合，参与涉及网格蛋白和肌动蛋白的多种膜运输途径。然而，对于许多货物的网格蛋白介导的内吞作用，CLC并非必需。在此我们观察到，CLC的缺失通过与Hip结合影响细胞迁移，并通过干扰无活性β1整合素正常内吞后的再循环，降低β1整合素的表面表达。CLC的缺失以及修饰型CLC的表达也会抑制旋转（G）-网格蛋白结构的出现，而G-网格蛋白结构是转铁蛋白受体从内体快速再循环的已知介质。修饰型CLC的表达减少了β1整合素和转铁蛋白受体的再循环以及细胞迁移，表明G-网格蛋白参与了这些过程。在子宫侵袭过程中，迁移的人滋养层细胞中CLC的CLCb亚型上调，这支持了CLC在迁移中的生理作用。总之，这些研究表明CLC介导了迁移过程中G-网格蛋白再循环所需的网格蛋白-肌动蛋白相互作用。
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