Filamin 2 (FLN2): A Muscle-specific Sarcoglycan Interacting Protein

Author:

Thompson Terri G.1,Chan Yiu-Mo1,Hack Andrew A.2,Brosius Melissa1,Rajala Michael1,Lidov Hart G.W.1,McNally Elizabeth M.23,Watkins Simon4,Kunkel Louis M.1

Affiliation:

1. Howard Hughes Medical Institute and Division of Genetics, Children’s Hospital and Harvard Medical School, Boston, Massachusetts 02115;

2. Department of Molecular Genetics and Cell Biology,

3. Department of Medicine, Section of Cardiology, University of Chicago, Chicago, Illinois 60637; and

4. Center for Biological Imaging, University of Pittsburgh, Pittsburgh, Pennsylvania 15261

Abstract

Mutations in genes encoding for the sarcoglycans, a subset of proteins within the dystrophin–glycoprotein complex, produce a limb-girdle muscular dystrophy phenotype; however, the precise role of this group of proteins in the skeletal muscle is not known. To understand the role of the sarcoglycan complex, we looked for sarcoglycan interacting proteins with the hope of finding novel members of the dystrophin–glycoprotein complex. Using the yeast two-hybrid method, we have identified a skeletal muscle-specific form of filamin, which we term filamin 2 (FLN2), as a γ- and δ-sarcoglycan interacting protein. In addition, we demonstrate that FLN2 protein localization in limb-girdle muscular dystrophy and Duchenne muscular dystrophy patients and mice is altered when compared with unaffected individuals. Previous studies of filamin family members have determined that these proteins are involved in actin reorganization and signal transduction cascades associated with cell migration, adhesion, differentiation, force transduction, and survival. Specifically, filamin proteins have been found essential in maintaining membrane integrity during force application. The finding that FLN2 interacts with the sarcoglycans introduces new implications for the pathogenesis of muscular dystrophy.

Publisher

Rockefeller University Press

Subject

Cell Biology

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