Dlg1-PTEN Interaction Regulates Myelin Thickness to Prevent Damaging Peripheral Nerve Overmyelination

• Type: Article in International Scientific Journal
• Date: 2010

Authors

Cotter, L (Author) Other; Ozcelik, M (Author) Other; Jacob, C (Author) Other; Pereira, JA (Author) Other; Locher, V (Author) Other; Baumann, R (Author) Other; Relvas, JB (Author) Other; Suter, U (Author) Other; Tricaud, N (Author) Other

Journal

Title: Science

Vol. 328

Pages: 1415-1418

ISSN: 0036-8075

Publisher: American Association for the Advancement of Science

Indexing

ISI Web of Knowledge - 116 Citations

Scopus - 127 Citations

Other information

Authenticus ID: P-003-5QZ

DOI: 10.1126/science.1187735

Abstract (EN): The thickness of the myelin sheath that insulates axons is fitted for optimal nerve conduction velocity. Here, we show that, in Schwann cells, mammalian disks large homolog 1 (Dlg1) interacts with PTEN (phosphatase and tensin homolog deleted on chromosome 10) to inhibit axonal stimulation of myelination. This mechanism limits myelin sheath thickness and prevents overmyelination in mouse sciatic nerves. Removing this brake results also in myelin outfoldings and demyelination, characteristics of some peripheral neuropathies. Indeed, the Dlg1 brake is no longer functional in a mouse model of Charcot-Marie-Tooth disease. Therefore, negative regulation of myelination appears to be essential for optimization of nerve conduction velocity and myelin maintenance.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 4