Control of rRNA transcription in liver of mice exposed to nutritional changes: initiation frequency may be a regulatory mechanism.
Shortly after feeding protein-depleted mice on a meal containing proteins, the RNA polymerase I activity in isolated liver nuclei shows a two fold to threefold activation over the basal value in nuclei of either normal or protein-depleted mice. This activation can be accounted for by the increase in the number of growing rRNA chains. Moreover, the template-bound RNA polymerase I fraction in nuclei from re-fed mice is about three times that from protein-depleted animals. An excess of template- unbound enzyme was found in liver nuclei from animals under either nutritional condition. Shortly after inhibition of protein synthesis by pactamycin administration to re-fed mice, the number of transcribing RNA polymerase I molecules in liver nuclei decreases to the basal level found in nuclei from protein-depleted mice, while in the latter, protein synthesis inhibition has no effect. These results support the suggestion that short-lived proteins may enhance the initiation frequency by RNA polymerase I after re-feeding.
D002467:Cell Nucleus / Q000201:enzymology; D004044:Dietary Proteins / Q000494:pharmacology; D007700:Kinetics; D008099:Liver / Q000201:enzymology; D011502:Protein-Energy Malnutrition / Q000378:metabolism*; D012318:RNA Polymerase I / Q000378:metabolism; D012335:RNA, Ribosomal / Q000235:genetics*; D014158:Transcription, Genetic / Q000187:drug effects; D014316:Tritium; D014544:Uridine Triphosphate / Q000378:metabolism
D004044:Dietary Proteins; D012335:RNA, Ribosomal; D014316:Tritium; D012318:RNA Polymerase I; D014544:Uridine Triphosphate