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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.

Genetics | Jul 21, 2003

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 RIS Download

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

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