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Defective dorsal closure and loss of epidermal decapentaplegic expression in Drosophila fos mutants
Author(s) -
Zeitlinger Julia,
Kockel Lutz,
Peverali Fiorenzo A.,
Jackson David B.,
Mlodzik Marek,
Bohmann Dirk
Publication year - 1997
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/16.24.7393
Subject(s) - decapentaplegic , biology , mutant , genetics , dorsum , drosophila (subgenus) , microbiology and biotechnology , drosophila melanogaster , gene , anatomy , imaginal disc
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 TGFβ‐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 .