Résumé
There is increasing evidence that at least some of the cellular homologues to retroviral oncogenes (c-
onc
or proto-oncogenes) are directly linked to the control of cell growth (for a review see ref. 1). Among these, c-
myc
, the cellular homologue to the avian myelocytomatosis virus (MC29) oncogene, has been shown to express high levels of mRNA during early G
0
/G
1
phase after mitogenic stimulation of T lymphocytes
2
by concanavalin A or of fibroblasts by platelet-derived growth factor (PDGF)
2
or serum
3
. An attractive model proposed for this regulation is that the c-
myc
gene is strongly repressed in cells arrested in the G
0
phase of the cell cycle by a growth factor-sensitive represser
4
. We have investigated an alternative model of post-transcriptional regulation. This latter model leads to two testable predictions. First, that c-
myc
mRNA should be unusually unstable, which we have confirmed
5
. And second, that there would be a high level of constitutive expression, a situation opposite to that implied by the represser model. Here we report that c-
myc
gene is indeed transcribed at a high rate in G
0
-arrested chinese hamster lung fibroblasts, although the level of mature c-
myc
mRNA is barely detectable. The early and dramatic increase in c-
myc
mRNA levels when these resting cells are stimulated by growth factors is not accompanied by any appreciable change in the transcription rate of c-
myc
gene. Taken together these findings support a model of post-transcriptional regulation of c-
myc
expression at the level of mRNA degradation.