Effect of the inhibition of nucleic acids and protein synthesis upon the development of melanotic tumors in Drosophila.
Ethidium bromide and chloramphenicol which inhibit the synthesis of DNA and of proteins in mitochondria, respectively, are devoid of any important effect on the development of melanotic tumors in Drosophila. Mitomycin C, added to the food of larvae carrying the tu48a mutant gene, increases the number and the size of tumors. It is effective only if the treatment is begun long before the appearance of the tumors and acts probably by weakening the defence reactions of the host. Actinomycin D, an inhibitor of RNA synthesis, increases the number of tumors most effectively if administered at the time of tumor gene activity. Cycloheximide, which is known to inhibit protein synthesis on cytoplasmic ribosomes, is effective during the entire larval life and increases the number of tumors. The results suggest that the melanotic tumor development in Drosophila is linked to the loss of cellular functions rather than to the acquisition of new ones.
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002701:Chloramphenicol / Q000494:pharmacology; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004331:Drosophila melanogaster; D004996:Ethidium / Q000494:pharmacology; D008545:Melanoma / Q000473:pathology*; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology; D009696:Nucleic Acids / Q000096:biosynthesis*; D014176:Protein Biosynthesis
D008937:Mitomycins; D009696:Nucleic Acids; D003609:Dactinomycin; D016685:Mitomycin; D002701:Chloramphenicol; D003513:Cycloheximide; D004996:Ethidium