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

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.

Role of Rho family GTPases in epithelial morphogenesis

“…It is well established that DJNK regulates the activity of several transcription factors. In particular, DJNK phosphorylates and activates Djun, which dimerizes with DFos to form a typical AP-1 complex (Hou et al 1997;Kockel et al 1997;RiesgoEscovar and Hafen 1997a,b;Zeitlinger et al 1997;Stronach and Perrimon 1999). DJNK also phosphorylates and inactivates the ETS-domain repressor Anterior open (Aop) (Riesgo-Escovar and Hafen 1997b).…”

Drosophila AP-1: lessons from an invertebrate

“…In addition, D-Fos serves as an e ector of JNK signaling during dorsal closure (see below; Zeitlinger et al, 1997;L Ciapponi, unpublished). Several of the characterized phosphorylation sites of c-Fos are conserved in D-Fos (Figure 1).…”

AP-1, but not NF-κB, is required for efficient steroid-triggered cell death in Drosophila

“…60 ± 62 Similarly, most kay alleles lead to embryonic lethality. However, kay 2 is a hypomorphic Dfos mutation that allows a few animals (*1%) to survive to adulthood, 63,66 allowing us to analyze the role of Dfos in larval salivary gland cell death. Control kay 2 /TM6B pupae displayed no defects in salivary gland cell death, with glands either partially or completely destroyed by 16 h after puparium formation ( Figure 5).…”

“…D59 was used to drive GAL4-dependent expression in larval salivary glands. 83 The dominant negative cactus BP4-DN125cactDPEST cDNA was kindly provided by D Stein, 70 the kay 2 mutant stock was provided by D Bohmann 63 and UAS-Fbz transformants were provided by M Bienz. 65 …”