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© The Rockefeller University Press, 0021-9525/2000//1009 $5.00
The Journal of Cell Biology, Volume 148, Number 5, , 2000 1009-1020

Original Article

Schwann Cell Myelination Requires Timely and Precise Targeting of P0 Protein



X. Yina, G.J. Kidda, L. Wrabetzb, M.L. Feltrib, A. Messingc, and B.D. Trappa

a Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195
b Department of Neurology and Department of Biological and Technological Research (DIBIT), San Raffaele Scientific Institute, 20132 Milano, Italy
c Waisman Center and Department of Pathobiological Sciences, School of Veterinary Medicine, University of Madison-Wisconsin, Madison, Wisconsin 53705
Department of Neurosciences, NC30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195.(216) 444 7927(216) 444 7177

trappb{at}ccf.org

This report investigated mechanisms responsible for failed Schwann cell myelination in mice that overexpress P0 (P0tg), the major structural protein of PNS myelin. Quantitative ultrastructural immunocytochemistry established that P0 protein was mistargeted to abaxonal, periaxonal, and mesaxon membranes in P0tg Schwann cells with arrested myelination. The extracellular leaflets of P0-containing mesaxon membranes were closely apposed with periodicities of compact myelin. The myelin-associated glycoprotein was appropriately sorted in the Golgi apparatus and targeted to periaxonal membranes. In adult mice, occasional Schwann cells myelinated axons possibly with the aid of endocytic removal of mistargeted P0. These results indicate that P0 gene multiplication causes P0 mistargeting to mesaxon membranes, and through obligate P0 homophilic adhesion, renders these dynamic membranes inert and halts myelination.

Key Words: PNS myelination • homophilic adhesion • dysmyelination • cell polarity • myelin protein gene dosage

© 2000 The Rockefeller University Press

Abbreviations used in this paper: CMT1A, Charcot-Marie-Tooth disease type 1A; CMT1B, Charcot-Marie-Tooth disease type 1B; CNP, 2',3' cyclic nucleotide 3'-phosphodiesterase; MAG, myelin-associated glycoprotein; MDL, major dense line; MT, microtubule; P0tg, TgN22Mes transgenic mice overexpressing P0 proteins; PLP, proteolipid protein; PMP22, peripheral myelin protein 22 kD; WT, wild-type.


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