Prohibitins Promote Proper Myelination

Impaired signaling between axons and Schwann cells leads to deficits in myelination and to axonal degradation, but investigating the signaling pathways at the axo-glial interface has proven to be technically challenging. Laura Feltri from the University of Buffalo in New York and colleagues have established a new model to study these juxtracrine, or contact-mediated, interactions. As reported in the Sep 18 Nature Communications, the researchers created a co-culture system with chambers containing axons and glia separated by a membrane, which enabled them to selectively isolate glial projections responding to axonal signaling. By conducting proteomic analysis of the glial leading edge, the researchers successfully identified a novel protein family required for myelination, called Prohibitins. Transgenic mice lacking Prohibitin-2 in glial cells exhibited impaired myelination and motor deficits. This technique could be applied to study other degenerative diseases, including ALS, where impaired communication between neurons and glia contributes to disease pathology.

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Poitelon Y, Bogni S, Matafora V, Della-Flora Nunes G, Hurley E, Ghidinelli M, Katzenellenbogen BS, Taveggia C, Silvestri N, Bachi A, Sannino A, Wrabetz L, Feltri ML. Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination. Nat Commun. 2015 Sep 18;6:8303. [Pubmed]

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