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  • The EMBO Journal (1997) 16, 7393 - 7401
  • doi:10.1093/emboj/16.24.7393

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

Julia Zeitlinger1, Lutz Kockel1, Fiorenzo A. Peverali2, David B. Jackson1, Marek Mlodzik1 and Dirk Bohmann1

  1. EMBL, Meyerhofstr. 1, 69117 Heidelberg, Germany
  2. IGBE-CNR, via Abbiategrasso 207, I-27100 Pavia, Italy

Correspondence to:

Marek Mlodzik, E-mail: mlodzik@embl-heidelberg.de

Dirk Bohmann, E-mail: bohmann@embl-heidelberg.de

Received 14 August 1997; Revised 2 October 1997

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.

  • Keywords:

    • Drosophila embryogenesis,
    • Fos,
    • Jun,
    • kayak,
    • dorsal closure