A transcriptional arrest mechanism involved in controlling constitutive levels of mouse c-myb mRNA

Oncogene. 1988 Mar;2(3):267-72.

Abstract

The control of c-myb mRNA abundance was examined in three representative cell lines, (the erythroleukaemia F4-12B2, the myeloma MOPC-31C and the fibroblast NIH3T3), which display abundant, low and undetectable levels of this transcript, respectively. We observed a small difference in half-life between F4-12B2 and MOPC-31C c-myb mRNA (175 min and 105 min, respectively) insufficient to account for the approximately 20-fold lower levels of this transcript in myelomas. Using the run-on transcription assay we found that c-myb transcripts were initiated at similar rates in all three cell types and were elongated at this relatively high rate to a site approximately 2 kilobases into the first intron. NIH3T3 c-myb transcripts did not proceed detectably beyond this pause/attenuation site, while in F4-12B2 cells transcription of regions 3' of this site occurred at a rate approximately 12-fold greater than in MOPC-31C. We have concluded that this transcriptional arrest mechanism, together with small differences in RNA turnover, were sufficient to account for the spectrum of c-myb mRNA abundance observed. Despite evidence of transcript initiation, we were unable to detect c-myb mRNA in fibroblasts, even under conditions (e.g. serum stimulation) which induced high c-myc mRNA levels. However, a novel 3.0 kilobase transcript with homology to c-myb was detected in cycloheximide-treated NIH3T3 cells.

MeSH terms

  • Animals
  • Cell Line
  • Cell Nucleus / metabolism
  • Fibroblasts / physiology
  • Gene Expression Regulation
  • In Vitro Techniques
  • Leukemia, Erythroblastic, Acute / genetics*
  • Mice
  • Plasmacytoma / genetics*
  • Proto-Oncogene Proteins / genetics*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Transcription, Genetic*

Substances

  • Proto-Oncogene Proteins
  • RNA, Messenger