Defective dorsal closure and loss of epidermal decapentaplegic expression in Drosophila fos mutants

EMBO J. 1997 Dec 15;16(24):7393-401. doi: 10.1093/emboj/16.24.7393.

Abstract

Drosophila kayak mutant embryos exhibit defects in dorsal closure, a morphogenetic cell sheet movement during embryogenesis. Here we show that kayak encodes D-Fos, the Drosophila homologue of the mammalian proto-oncogene product, c-Fos. D-Fos is shown to act in a similar manner to Drosophila Jun: in the cells of the leading edge it is required for the expression of the TGFbeta-like Decapentaplegic (Dpp) protein, which is believed to control the cell shape changes that take place during dorsal closure. Defects observed in mutant embryos, and adults with reduced Fos expression, are reminiscent of phenotypes caused by 'loss of function' mutations in the Drosophila JNKK homologue, hemipterous. These results indicate that D-Fos is required downstream of the Drosophila JNK signal transduction pathway, consistent with a role in heterodimerization with D-Jun, to activate downstream targets such as dpp.

MeSH terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Dimerization
  • Drosophila / embryology*
  • Drosophila / genetics*
  • Drosophila Proteins*
  • Embryo, Nonmammalian / physiology*
  • Epidermis / physiology
  • Gene Expression Regulation, Developmental
  • Genes, fos*
  • Insect Proteins / biosynthesis
  • Insect Proteins / genetics*
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases*
  • Models, Biological
  • Mutation
  • Phenotype
  • Proto-Oncogene Proteins c-fos / biosynthesis
  • Proto-Oncogene Proteins c-fos / genetics
  • Signal Transduction
  • Transforming Growth Factor beta

Substances

  • Drosophila Proteins
  • Insect Proteins
  • Proto-Oncogene Proteins c-fos
  • Transforming Growth Factor beta
  • dpp protein, Drosophila
  • Calcium-Calmodulin-Dependent Protein Kinases
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases