Superinduction of ornithine decarboxylase (ODC) by actinomycin D is due to stimulation of ODC mRNA translation.
Inhibition of transcription by treatment with actinomycin D caused superinduction of the ornithine decarboxylase (ODC) activity in Ehrlich ascites tumor cells. Experiments with cycloheximide ruled out the possibility that this superinduction was due to stabilization of ODC. Instead the ODC activity exhibited a more rapid turnover in the presence of actinomycin D (t1/2 = 56 min). The superinduction was found to coincide with an increased rate of ODC synthesis, as determined by measuring the incorporation of [35S )methionine into immunoreactive ODC protein. The steady-state level of ODC mRNA was unchanged, indicating an effect on the translational efficiency.
Wallon
U M
UM
Department of Zoophysiology, University of Lund, Sweden.
Persson
L
L
Heby
O
O
D000818:Animals; D003609:Dactinomycin / Q000494:pharmacology*; D004790:Enzyme Induction / Q000187:drug effects; D015870:Gene Expression / Q000187:drug effects; D066298:In Vitro Techniques; D051379:Mice; D009955:Ornithine Decarboxylase / Q000096:biosynthesis* / Q000235:genetics; D014176:Protein Biosynthesis / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D014407:Tumor Cells, Cultured
D012333:RNA, Messenger; D003609:Dactinomycin; D009955:Ornithine Decarboxylase