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Cell Growth & Differentiation, Vol 4, Issue 5 421-430, Copyright © 1993 by American Association of Cancer Research


ARTICLES

Posttranscriptional control of thymidine kinase messenger RNA accumulation in cells released from G0-G1 phase blocks

JM Gudas, JL Fridovich-Keil and AB Pardee
Division of Cell Growth and Regulation, Dana Farber Cancer Institute, Boston, Massachusetts 02115.

In this study, we have utilized thymidine kinase (TK) mRNA induction as a model for investigating regulatory events at the G1-S boundary of the cell cycle. Using three independent methods for synchronizing diploid, nontumorigenic CHEF/18 cells, we found that the mechanism(s) underlying TK mRNA accumulation varied with the method of cell synchrony used. When cells were arrested by serum deprivation, both transcriptional and posttranscriptional controls contributed to the observed accumulation of TK mRNA at the G1-S boundary. When synchronized by isoleucine deprivation, mature TK mRNA and TK pre-mRNAs increased significantly at the G1-S boundary of the cell cycle with no detectable change in the rate of TK gene transcription. Following lovastatin treatment, which appears to arrest cells at a point very early in G1, posttranscriptional mechanisms were solely responsible for the subsequent accumulation of TK mRNA observed upon mevalonate repletion. We confirmed that transcriptional mechanisms were involved in TK mRNA regulation only when cells progressed from G0 into S phase using reporter genes transcribed from the heterologous human TK promoter. Taken together, these results indicate that posttranscriptional mechanism(s) are primarily responsible for regulating the abundance of TK mRNA during the cell cycle in CHEF/18 cells and further suggest uncoupling of transcriptional and posttranscriptional controls following different physiological conditions of cell cycle arrest.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1993 by the American Association of Cancer Research.