Response of Djun and Dfos mRNA abundance to signal transduction pathways in cultured cells of Drosophila melanogaster.
The mammalian proto-oncogenes c-jun and c-fos are situated at the end of multiple signal transduction pathways and activation of their products Jun and Fos, components of the transcription factor AP-1, are able to regulate gene transcription in response to extracellular stimuli. Djun and Dfos, the products of the Drosophila proto-oncongenes Djun and Dfos, are similar in size and sequence to their mammalian counterparts c-Jun and c-Fos and are related to their mammalian counterparts by their antigenic properties. However, very little is known about how they are regulated through signal transduction pathways. This paper has investigated the response of their mRNA abundance levels to three signal transduction pathways in Drosophila cultured cells. Various agonists and antagonists that stimulate and inhibit specific enzymes in the pathways have been tested. The results suggest that Djun and Dfos mRNA are continuously expressed and their abundance levels are transiently regulated by multiple signaling pathways, the peak response coming at 1-2 hours after perturbation. Dfos is more highly regulated than Djun which is only modulated. The receptor tyrosine kinase pathways positively regulate Dfos and Djun. The cAMP-mediated pathway positively regulates Dfos but negatively regulates Djun. The protein kinase C-activated pathway does not affect Djun whereas it negatively regulates Dfos.
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Department of Biology, Arizona State University, Tempe 85287-1501, USA.
Goldstein
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D000818:Animals; D002478:Cells, Cultured / Q000201:enzymology / Q000502:physiology; D017077:Culture Media, Conditioned / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism / Q000502:physiology; D004330:Drosophila / Q000166:cytology / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D018507:Gene Expression Regulation, Developmental; D017344:Genes, Insect / Q000235:genetics / Q000502:physiology; D016762:Genes, fos / Q000235:genetics / Q000502:physiology; D016758:Genes, jun / Q000235:genetics / Q000502:physiology; D019476:Insect Proteins / Q000235:genetics* / Q000502:physiology; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D010744:Phosphoric Monoester Hydrolases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000494:pharmacology; D011518:Proto-Oncogene Proteins / Q000235:genetics* / Q000502:physiology; D012333:RNA, Messenger / Q000187:drug effects* / Q000235:genetics* / Q000378:metabolism; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000494:pharmacology / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics* / Q000502:physiology
D017077:Culture Media, Conditioned; D019476:Insect Proteins; D010726:Phosphodiesterase Inhibitors; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D000242:Cyclic AMP; D020794:Receptor Protein-Tyrosine Kinases; D017346:Protein Serine-Threonine Kinases; D011493:Protein Kinase C; D010744:Phosphoric Monoester Hydrolases