Glucocorticoid regulation of thymidine kinase (Tk-1) expression in L929 cells

G. H. Frost, K. Rhee, E. A. Thompson

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

Glucocorticoids regulate the proliferation of mouse L cells. Incorporation of [3H]thymidine is inhibited by 70-90% within 24 h after addition of 0.1 μM dexamethasone. This effect on L cells is completely reversible. The expression of the thymidine kinase gene (Tk-1) has been examined in L cells that have been treated with 0.1 μM dexamethasone for 24 h. Dexamethasone inhibits thymidine kinase activity 70-90% after 24 h. This is associated with a 90-95% decrease in Tk mRNA abundance. The decrease in Tk mRNA is not caused by a decrease in transcription of Tk-1, as shown by nuclear run-on transcription assays. Transient expression of the CAT (chloramphenicol acetyltransferase) gene, driven by the Tk-1 promoter, was not affected by dexamethasone, and transcription of stably integrated Tk minigenes in LMTk- cells was not affected by dexamethasone. This effect was observed regardless of whether Tk cDNA was fused to the simian virus 40 promoter or the mouse Tk- 1 promoter region. Conversely, expression of thymidine kinase was inhibited when stable Tk+ transformants of LMTk- cells were exposed to glucocorticoids; and inhibition of expression was observed irrespective of the promoter that was used to drive transcription of the Tk minigenes. These data indicate that glucocorticoid regulation of Tk-1 in mouse L cells is, within the limits of detection of the assays used in these studies, entirely due to a posttranscriptional mechanism.

Original languageEnglish (US)
Pages (from-to)6748-6754
Number of pages7
JournalJournal of Biological Chemistry
Volume268
Issue number9
StatePublished - Jan 1 1993

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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