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A cuticle collagen encoded by the lon-3 gene may be a target of TGF-beta signaling in determining Caenorhabditis elegans body shape.

The signaling pathway initiated by the TGF-beta family member DBL-1 in Caenorhabditis elegans controls body shape in a dose-dependent manner. Loss-of-function (lf) mutations in the dbl-1 gene cause a short, small body (Sma phenotype), whereas overexpression of dbl-1 causes a long body (Lon phenotype). To understand the cellular mechanisms underlying these phenotypes, we have isolated suppressors of the Sma phenotype resulting from a dbl-1(lf) mutation. Two of these suppressors are mutations in the lon-3 gene, of which four additional alleles are known. We show that lon-3 encodes a collagen that is a component of the C. elegans cuticle. Genetic and reporter-gene expression analyses suggest that lon-3 is involved in determination of body shape and is post-transcriptionally regulated by the dbl-1 pathway. These results support the possibility that TGF-beta signaling controls C. elegans body shape by regulating cuticle composition.

Pubmed ID: 12524338

Authors

  • Suzuki Y
  • Morris GA
  • Han M
  • Wood WB

Journal

Genetics

Publication Data

December 13, 2002

Associated Grants

  • Agency: NICHD NIH HHS, Id: HD-14958
  • Agency: NIGMS NIH HHS, Id: R01 GM047869

Mesh Terms

  • Animals
  • Base Sequence
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins
  • Collagen
  • DNA, Helminth
  • Genes, Helminth
  • Genes, Reporter
  • Green Fluorescent Proteins
  • Luminescent Proteins
  • Models, Biological
  • Molecular Sequence Data
  • Mutation
  • Phenotype
  • Protein Processing, Post-Translational
  • Recombinant Fusion Proteins
  • Signal Transduction
  • Suppression, Genetic
  • Transforming Growth Factor beta