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Published 13 May 2002. doi:10.1083/jcb.200201063
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© The Rockefeller University Press, 0021-9525/2002/5/679 $5.00
The Journal of Cell Biology, Volume 157, Number 4, May 13, 2002 679-691

Article

 Pincher, a pinocytic chaperone for nerve growth factor/TrkA signaling endosomes

Yufang Shao1, Wendy Akmentin1, Juan Jose Toledo-Aral1, Julie Rosenbaum1, Gregorio Valdez1, John B. Cabot1, Brian S. Hilbush2 and Simon Halegoua1

1 Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, NY 11794
2 Digital Gene Technologies Inc., La Jolla, CA 92037

Address correspondence to Simon Halegoua, Dept. of Neurobiology and Behavior, Life Sciences Bldg. 052, SUNY at Stony Brook, Stony Brook, NY 11794-5230. Tel.: (631) 632-8736. Fax: (631) 632-9714. E-mail: simon.halegoua{at}sunysb.edu

Acentral tenet of nerve growth factor (NGF) action that is poorly understood is its ability to mediate cytoplasmic signaling, through its receptor TrkA, that is initiated at the nerve terminal and conveyed to the soma. We identified an NGF-induced protein that we termed Pincher (pinocytic chaperone) that mediates endocytosis and trafficking of NGF and its receptor TrkA. In PC12 cells, overexpression of Pincher dramatically stimulated NGF-induced endocytosis of TrkA, unexpectedly at sites of clathrin-independent macropinocytosis within cell surface ruffles. Subsequently, a system of Pincher-containing tubules mediated the delivery of NGF/TrkA-containing vesicles to cytoplasmic accumulations. These vesicles selectively and persistently mediated TrkA-erk5 mitogen-activated protein kinase signaling. A dominant inhibitory mutant form of Pincher inhibited the NGF-induced endocytosis of TrkA, and selectively blocked TrkA-mediated cytoplasmic signaling of erk5, but not erk1/2, kinases. Our results indicate that Pincher mediates pinocytic endocytosis of functionally specialized NGF/TrkA endosomes with persistent signaling potential.

Key Words: neutrophin; membrane trafficking; signal transduction; EH domain; MAP kinase


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