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PMID: 14962982 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

ZZ domain is essentially required for the physiological binding of dystrophin and utrophin to beta-dystroglycan.

Human molecular genetics ·Vol. 13 ·No. 7 ·2004-04-01 ·Pages 693-702

Ishikawa-Sakurai M, Yoshida M, Imamura M, Davies KE, Ozawa E

Abstract

An intracellular protein, dystrophin, plays an important role in keeping muscle fibers intact by binding at its N-terminal end to the subsarcolemmal cytoskeletal actin network and via its C-terminal end to the transmembraneous protein beta-dystroglycan. Duchenne muscular dystrophy is caused by the loss of dystrophin, which can result from the loss of this binding. The N-terminal part of the latter binding site of dystrophin has been well documented using overlay assay and X-ray diffraction assays. However, the binding site at the C-terminal region of dystrophin has not been examined in detail. In the present work, we report a detailed analysis of the C-terminal binding domain as follows. (1). The full binding activity corresponding to the effective binding in vivo is expressed by the dystrophin fragment spanning amino acids 3026-3345 containing the ZZ domain at the C-terminus. Determination of this binding range is important not only for understanding of the mechanism of dystrophy, but also useful for the design of truncated dystrophin constructs for gene therapy. (2). The ZZ domain binds to EF1 domain in the dystrophin fragment to reinforce the binding activity. (3). The cysteine 3340 in the ZZ domain is essential for the binding of dystrophin to beta-dystroglycan. A reported case of DMD due to missense mutation C3340Y may be caused by inability to fix dystrophin beneath the cell membrane. (4). The binding mode of utrophin is different from that of dystrophin. The difference is conspicuous concerning the cysteine residues present in the ZZ domain.

MeSH Terms
Amino Acid Sequence Binding Sites DNA, Complementary/metabolism Dose-Response Relationship, Drug Dystroglycans/chemistry Dystrophin/chemistry Escherichia coli/metabolism Glutathione Transferase/metabolism Humans Models, Biological Models, Genetic Molecular Sequence Data Mutation Mutation, Missense Phenotype Protein Binding Protein Structure, Tertiary Recombinant Fusion Proteins/metabolism Recombinant Proteins/chemistry Sequence Homology, Amino Acid Utrophin/chemistry
Chemicals
DNA, Complementary Dystrophin Recombinant Fusion Proteins Recombinant Proteins Utrophin Dystroglycans Glutathione Transferase
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Ishikawa-Sakurai Michiko
Department of Cell Biology, National Institute of Neuroscience, Tokyo, Japan.
Yoshida Mikiharu
Imamura Michihiro
Davies Kay E
Ozawa Eijiro
Article Info
Journal
Human molecular genetics
Abbr.
Hum Mol Genet
ISSN
0964-6906
Published
2004-04-01
Epub
2004-00-12
Pages
693-702
Language
English
Region
England
NLM ID
9208958
Subset
IM
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