Mechanisms for the control of body size by a G-kinase and a downstream TGFbeta signal pathway in Caenorhabditis elegans

Genes Cells. 2004 Jan;9(1):39-47. doi: 10.1111/j.1356-9597.2004.00700.x.


We recently showed that egl-4 mutants in Caenorhabditis elegans have a much larger body size and that the egl-4 gene encodes cyclic GMP-dependent protein kinases (G-kinases). Cell sizes, but not cell numbers, in the major organs are increased in the mutants. Genetic interaction studies suggest that EGL-4 represses the DBL-1/TGFbeta pathway that is known to control body size. To understand the mechanisms of body size control in C. elegans, we analysed sma-2, sma-4 and sma-6 small mutants in the DBL-1 pathway. The volumes of major organs were precisely determined with the method developed by us. They are significantly decreased as compared to those of the wild-type while cell numbers are not, indicating that cell size is decreased. DNA contents in the nuclei of major organs are not significantly changed in the small mutants and in an egl-4 large mutant. Total protein contents are much decreased in the small mutants and slightly increased in the egl-4 mutant. Based on these results, we propose that decreased cell and body size of the small mutants in the DBL-1/TGFbeta pathway is mainly due to decreased levels of protein expression, and that increase in fluid content is a major reason for the increase in cell and body size in egl-4 mutants.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Body Constitution / physiology*
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins / genetics
  • Caenorhabditis elegans Proteins / metabolism
  • Cell Count
  • Cell Nucleus / genetics
  • Cell Nucleus / metabolism
  • Cyclic GMP-Dependent Protein Kinase Type I
  • Cyclic GMP-Dependent Protein Kinases / genetics
  • Cyclic GMP-Dependent Protein Kinases / metabolism*
  • DNA / metabolism
  • Mutation
  • Neuropeptides / genetics
  • Neuropeptides / metabolism
  • Osmotic Pressure
  • Signal Transduction / physiology*
  • Sodium Chloride / metabolism
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / metabolism*


  • Caenorhabditis elegans Proteins
  • Dbl-1 protein, C elegans
  • Neuropeptides
  • Transforming Growth Factor beta
  • Sodium Chloride
  • DNA
  • Cyclic GMP-Dependent Protein Kinase Type I
  • Cyclic GMP-Dependent Protein Kinases
  • EGL-4 protein, C elegans