Molecular and General Genetics MGG

, Volume 242, Issue 3, pp 346–357

The Caenorhabditis elegans unc-60 gene encodes proteins homologous to a family of actin-binding proteins

Authors

  • Kim S. McKim
    • Institute of Molecular Biology and Biochemistry, Department of Biological SciencesSimon Fraser University
  • Camela Matheson
    • Institute of Molecular Biology and Biochemistry, Department of Biological SciencesSimon Fraser University
  • Marco A. Marra
    • Institute of Molecular Biology and Biochemistry, Department of Biological SciencesSimon Fraser University
  • Marcia F. Wakarchuk
    • Institute of Molecular Biology and Biochemistry, Department of Biological SciencesSimon Fraser University
  • David L. Baillie
    • Institute of Molecular Biology and Biochemistry, Department of Biological SciencesSimon Fraser University
Originals Articles

DOI: 10.1007/BF00280425

Cite this article as:
McKim, K.S., Matheson, C., Marra, M.A. et al. Molec. Gen. Genet. (1994) 242: 346. doi:10.1007/BF00280425

Abstract

Mutations in the unc-60 gene of the nematode Caenorhabditis elegans result in paralysis. The thin filaments of the muscle cells are severely disorganized and not bundled with myosin into functional contractile units. Here we report the cloning and sequence of unc-60. Two unc-60 transcripts, 1.3 and 0.7 kb in size, were detected. The transcripts share a single exon encoding only the initial methionine, yet encode proteins with homologous sequences. The predicted protein products are 165 and 152 amino acids in length and their sequences are 38% identical. Both proteins are homologous to a family of actin depolymerizing proteins identified in vertebrate, plant and protozoan systems. We propose that the unc-60 locus encodes proteins that depolymerize growing actin filaments in muscle cells, and that these proteins are required for the assembly of actin filaments into the contractile myofilament lattice of C. elegans muscle. unc-60 has an essential function in development, since one unc-60 allele, s1586, has a recessive lethal phenotype. Our characterization of s1586 has shown that it is a small deletion which disrupts both coding regions.

Key words

Caenorhabditis elegansunc-60MuscleActin-binding protein
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Copyright information

© Springer-Verlag 1994