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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Ribonucleotide reductase gene expression during cyclic AMP-induced cell cycle arrest in T lymphocytes.

In both 3T3 mouse fibroblasts and S49 mouse T lymphocytes the genes encoding both subunits of ribonucleotide reductase are expressed beginning in late G1 phase. In studies reported here, we compared the expression of the genes that code for the M1 and M2 subunits of ribonucleotide reductase in S49 cells, which are arrested in G1 phase by agents that increase cyclic AMP, with those from CEM human T lymphoma cells that are unaffected by exposure to dibutyryl cyclic AMP. Dibutyryl cyclic AMP treatment results in a prompt steady diminution of M2 mRNA concentration to levels at or below that of elutriated G1 cell-cycle-specific populations in S49 cells, in contrast to CEM cell M2 mRNA, which is unchanged. M1 mRNA concentration decreases more slowly than M2 mRNA in S49 cells and marginally, if at all, in CEM cells. The time course of diminution of the M2 message concentration by dibutyryl cyclic AMP in S49 cells is similar to that obtained when cells are treated with actinomycin D and to the combination of the two agents. This suggests that cyclic AMP and actinomycin D may act similarly on ribonucleotide reductase gene expression. Furthermore, cycloheximide pretreatment diminishes the effect of dibutyryl cyclic AMP, indicating that the effect might be mediated by a labile protein. Transcription runoff assays suggest a diminution of transcription rate for the M2 gene in S49 cells treated with dibutyryl cyclic AMP and a transient decline in the M1 transcription rate. These data suggest that dibutyryl cyclic AMP diminishes the transcription of ribonucleotide reductase genes in sensitive cells and that this and the short half-life of the M2 message are major factors in the disappearance of the M2 messenger RNA from dibutyryl cyclic AMP-treated cells although other mechanisms may also play a role. These events clearly precede any alteration in cell cycle distribution and thus they may contribute to G1 arrest.[1]

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