unc-53 controls longitudinal migration in C. elegans

Development. 2002 Jul;129(14):3367-79.


Cell migration and outgrowth are thought to be based on analogous mechanisms that require repeated cycles of process extension, reading and integration of multiple directional signals, followed by stabilisation in a preferred direction, and renewed extension. We have characterised a C. elegans gene, unc-53, that appears to act cell autonomously in the migration and outgrowth of muscles, axons and excretory canals. Abrogation of unc-53 function disrupts anteroposterior outgrowth in those cells that normally express the gene. Conversely, overexpression of unc-53 in bodywall muscles leads to exaggerated outgrowth. UNC-53 is a novel protein conserved in vertebrates that contains putative SH3- and actin-binding sites. unc-53 interacts genetically with sem-5 and we demonstrated a direct interaction in vitro between UNC-53 and the SH2-SH3 adaptor protein SEM-5/GRB2. Thus, unc-53 is involved in longitudinal navigation and might act by linking extracellular guidance cues to the intracellular cytoskeleton.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Amino Acid Sequence
  • Animals
  • Animals, Genetically Modified
  • Base Sequence
  • Body Patterning / genetics
  • Caenorhabditis elegans / genetics*
  • Caenorhabditis elegans / growth & development*
  • Caenorhabditis elegans Proteins / genetics*
  • Cell Movement / genetics
  • Chromosome Mapping
  • DNA, Helminth / genetics
  • Female
  • Gene Expression Regulation, Developmental
  • Genes, Helminth*
  • Male
  • Microfilament Proteins / genetics*
  • Models, Biological
  • Molecular Sequence Data
  • Muscles / cytology
  • Mutation
  • Phenotype
  • Sequence Homology, Amino Acid


  • Caenorhabditis elegans Proteins
  • DNA, Helminth
  • Microfilament Proteins
  • UNC-53 protein, C elegans