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Further Evidence against Post-transcriptional Control of Inducible Tyrosine Aminotransferase Synthesis in Cultured Hepatoma Cells


THE paradoxical increase in concentration of specific proteins following treatment with inhibitors of macromolecular synthesis, a phenomenon sometimes termed ‘superinduction’, is rather frequently observed in eukaryotic cells. Tomkins et al.1 listed some eighty reported observations of this kind that have been made in bacterial, plant, and animal systems and, while acknowledging that the mechanism involved has been analysed in only a few of these, argued that the frequency of effects of this kind in mammalian cells suggests that control of gene expression by post-transcriptional mechanisms is quite common. This suggestion stems from their analyses of the effects of actinomycin D on the inducible tyrosine amino- transferase in cultured hepatoma cells. These analyses have led to elaboration of a model involving a labile cytoplasmic repressor, which reversibly inhibits the translation of amino-transferase mRNA (ref. 2) and/or promotes mRNA degradation3. In this view, steroid-mediated induction can be attributed to inhibition by the hormone of either the synthesis or the activity of repressor. If correct, this model quite properly focuses attention on post-transcriptional control mechanisms as of primary interest in steroid-mediated enzyme induction and, by extension, in other mammalian regulatory systems as well.

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KENNEY, F., LEE, KL., STILES, C. et al. Further Evidence against Post-transcriptional Control of Inducible Tyrosine Aminotransferase Synthesis in Cultured Hepatoma Cells. Nature New Biology 246, 208–210 (1973).

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