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Showing papers by "Julia Zeitlinger published in 1997"


Journal ArticleDOI
TL;DR: The redundant function of Jun in eye development may contribute to the precision of photoreceptor differentiation and ommatidial assembly and be uncovered by mutations in other signaling components.
Abstract: Drosophila Jun is shown to be involved in different signal transduction pathways and developmental decisions. Dorsal closure, a morphogenetic process occurring during Drosophila embryogenesis, is regulated by Hemipterous (Hep) and Basket (Bsk), homologs of JNKK and JNK, respectively. Embryos lacking Jun activity exhibit a dorsal closure phenotype, very similar to that of bsk and hep mutants, indicating that Jun is a target of Hep/Bsk signaling. In eye and wing development Jun participates in a separate signaling pathway that is comprised of Ras, Raf, and the ERK-type kinase Rolled. In contrast to the strict requirement for Jun in dorsal closure, its role in the eye is redundant but can be uncovered by mutations in other signaling components. The redundant function of Jun in eye development may contribute to the precision of photoreceptor differentiation and ommatidial assembly.

148 citations


Journal ArticleDOI
TL;DR: 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.
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.

118 citations