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J Cell Biol. 2000 May 15;149(4):931-42.

Mutations in beta-spectrin disrupt axon outgrowth and sarcomere structure.

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  • 1Department of Biology, University of Utah, Salt Lake City 84112-0840, USA.

Abstract

beta-Spectrin is a major component of the membrane skeleton, a structure found at the plasma membrane of most animal cells. beta-Spectrin and the membrane skeleton have been proposed to stabilize cell membranes, generate cell polarity, or localize specific membrane proteins. We demonstrate that the Caenorhabditis elegans homologue of beta-spectrin is encoded by the unc-70 gene. unc-70 null mutants develop slowly, and the adults are paralyzed and dumpy. However, the membrane integrity is not impaired in unc-70 animals, nor is cell polarity affected. Thus, beta-spectrin is not essential for general membrane integrity or for cell polarity. However, beta-spectrin is required for a subset of processes at cell membranes. In neurons, the loss of beta-spectrin leads to abnormal axon outgrowth. In muscles, a loss of beta-spectrin leads to disorganization of the myofilament lattice, discontinuities in the dense bodies, and a reduction or loss of the sarcoplasmic reticulum. These defects are consistent with beta-spectrin function in anchoring proteins at cell membranes.

PMID:
10811832
[PubMed - indexed for MEDLINE]
PMCID:
PMC2174563
Free PMC Article

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