DEFECTIVE DORSAL CLOSURE AND LOSS OF EPIDERMAL DECAPENTAPLEGIC EXPRESSION IN DROSOPHILA FOS MUTANTS

Drosophila kayak mutant embryos exhibit defects in dorsal closure, a m orphogenetic cell sheet movement during embryogenesis. Here we show th at kayak encodes D-Fos, the Drosophila homologue of the mammalian prot o-oncogene product, c-Fos. D-Fos is shown to act in a similar manner t o Drosophila Jun: in the cells of the leading edge it is required for the expression of the TGF beta-like Decapentaplegic (Dpp) protein, whi ch is believed to control the cell shape changes that take place durin g 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 Drosop hila JNK signal transduction pathway, consistent with a role in hetero dimerization with D-Jun, to activate downstream targets such as dpp.