Regulation of rRNA synthesis in human and mouse cells is not determined by changes in active gene count

Cell Cycle. 2006 Apr;5(7):735-9. doi: 10.4161/cc.5.7.2633. Epub 2006 Apr 1.

Abstract

Growth regulation of the tandemly repeated ribosomal RNA (rRNA) genes in mammals can potentially occur by several distinct mechanisms. Only a fraction of the 200 or so rRNA genes appears to be activated in somatic cells, leaving open the possibility that enhanced transcription could result from gene activation events. Here we have determined the active rRNA gene count after growth stimulation with EGF, direct Raf activation and chromatin hyperacetylation and after inhibiting MAP-kinase signaling. Despite robust changes in rRNA transcription rates, we find no significant variation in active gene number in either mouse fibroblasts or human neuroepithelioma cells. Interestingly, the data also show that rRNA transcription enhancement induced by hyperacetylation is dependent on MEK/ERK signaling. Since ERK and the acetyltransferase CBP both bind the architectural factor UBF, this suggests a mechanism for targeting active CBP to the rRNA genes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation / drug effects
  • Animals
  • Enzyme Activation / drug effects
  • Epidermal Growth Factor / pharmacology
  • Gene Dosage / genetics*
  • Gene Expression Regulation*
  • Humans
  • Hydroxamic Acids / pharmacology
  • Mice
  • NIH 3T3 Cells
  • RNA, Ribosomal / biosynthesis*
  • RNA, Ribosomal / genetics
  • Transcriptional Activation
  • Tumor Cells, Cultured
  • raf Kinases / metabolism

Substances

  • Hydroxamic Acids
  • RNA, Ribosomal
  • trichostatin A
  • Epidermal Growth Factor
  • raf Kinases