Clathrin light chains are required for the gyrating-clathrin recycling pathway and thereby promote cell migration

Sophia R. Majeed, Lavanya Vasudevan, Chih-Ying Chen, Yi Luo, Jorge A. Torres, Timothy M. Evans, Andrew Sharkey, Amy B. Foraker, Nicole M. L. Wong, Christopher Esk, Alan Freeman, Ashley Moffett, James H. Keen and Frances M. Brodsky ()
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Sophia R. Majeed: University of California San Francisco
Lavanya Vasudevan: University of California San Francisco
Chih-Ying Chen: University of California San Francisco
Yi Luo: Thomas Jefferson University
Jorge A. Torres: University of California San Francisco
Timothy M. Evans: University of California San Francisco
Andrew Sharkey: University of Cambridge
Amy B. Foraker: University of California San Francisco
Nicole M. L. Wong: University of California San Francisco
Christopher Esk: University of California San Francisco
Ashley Moffett: University of Cambridge
James H. Keen: Thomas Jefferson University
Frances M. Brodsky: University of California San Francisco

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract 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.

Date: 2014
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DOI: 10.1038/ncomms4891

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