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Human Molecular Genetics Advance Access originally published online on June 2, 2004
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Human Molecular Genetics, 2004, Vol. 13, No. 15 1657-1668
DOI: 10.1093/hmg/ddh170
Human Molecular Genetics, Vol. 13, No. 15 © Oxford University Press 2004; all rights reserved

Ezrin-dependent regulation of the actin cytoskeleton by ß-dystroglycan

H.J. Spence1, Y.-J. Chen2, C.L. Batchelor3, J.R. Higginson2,3, H. Suila4, O. Carpen4 and S.J. Winder3,*

1CRUK Beatson Laboratories, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK, 2Institute of Biomedical and Life Sciences, Davidson Building, University of Glasgow, Glasgow G12 8QQ, UK, 3Centre for Developmental Genetics, Department of Biomedical Science, University of Sheffield, Western Bank, Sheffield S10 2TN, UK and 4Department of Pathology and Neuroscience Program, Biomedicum, 5th floor and Helsinki University Central Hospital, Haartmaninkatu, PO Box 63 (Haartmaninkatu 8), University of Helsinki, 00014 Helsinki, Finland

Received April 6, 2004; Accepted May 21, 2004

Dystroglycan is part of an adhesion receptor complex linking the extracellular matrix to the actin cytoskeleton. Previous studies have implicated dystroglycan in basement membrane formation and as a crucial link between dystrophin and laminin in muscle. We report here a further novel function for dystroglycan which appears to be in addition to its role as an adhesion molecule. ß-dystroglycan has been localized to microvilli structures in a number of cell types where it associates with the cytoskeletal adaptor ezrin, through which it is able to modulate the actin cytoskeleton and induce peripheral filopodia and microvilli. Ezrin is able to interact with dystroglycan through a cluster of basic residues in the juxtamembrane region of dystroglycan, and mutation of these residues both prevents ezrin binding and the induction of actin-rich surface protrusions. These studies reveal novel functions and additional signalling roles for dystroglycan, raising the possibility of new avenues for therapeutic intervention in diseases such as Duchenne muscular dystrophy.

* To whom correspondence should be addressed. Tel: +44 1142222332; Fax: +44 1142765413; Email: s.winder{at}sheffield.ac.uk


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