Transcription of Dfos is stimulated by brain tumours of l(2)gl-deficient larvae of Drosophila melanogaster.
Mutations in the tumour suppressor gene l(2)gl cause formation of brain and imaginal disc tumours. The product of this gene was suggested to be a part of an intercellular communication system, regulating cell growth and differentiation. Oncogenic activation of many signalling pathways, involved in similar processes, result in increased activity of the AP-1 family of transcription factors. In this paper we explored the interaction between the cancer mutation l(2)gl and the level of transcription of the AP-1 proteins. We report that in brain tumours from l(2)gl-deficient larvae, transcription of the Drosophila melanogaster c-fos homologue was stimulated but that of the c-jun homologue was unchanged. Our results provide further evidence that the protein l(2)gl is a component of a signalling pathway, a nuclear target of which is the AP-1 family of transcription factors.
Nedelcheva
M
M
Department of Genetics, Faculty of Biology, University of Sofia, 8 Dragan Tsankov Str., 1421 Sofia, Bulgaria.
Topouzova
T
T
Genova
G
G
D000818:Animals; D001921:Brain / Q000378:metabolism; D001932:Brain Neoplasms / Q000235:genetics*; D002467:Cell Nucleus / Q000378:metabolism; D004331:Drosophila melanogaster / Q000196:embryology* / Q000235:genetics*; D016762:Genes, fos / Q000235:genetics*; D017403:In Situ Hybridization; D017404:In Situ Hybridization, Fluorescence; D009154:Mutation; D010957:Plasmids / Q000378:metabolism; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism; D015398:Signal Transduction; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014158:Transcription, Genetic
D016755:Proto-Oncogene Proteins c-jun; D018808:Transcription Factor AP-1