The levels of thymosin beta 4 mRNA were studied throughout the cell cy
cle of NIH 3T3 cells. In serum deprived, quiescent cells, the levels o
f thymosin beta 4 were undetectable; after serum restoration, the cell
s were induced to proliferate and we found a pronounced increase in th
ymosin beta 4 mRNA levels at the G(1)/S transition. Thymosin beta 4 mR
NA was induced even in the presence of cycloheximide. On the other han
d, cycling cells that were synchronized at different stages of the cyc
le by means of mitotic shake-off after nocodazole arrest or a double t
hymidine block did not show any variation in the levels of thymosin be
ta 4 mRNA when they progressed synchronously through the cycle. In con
clusion, the present data indicate that the thymosin beta 4 gene is re
gulated by cell proliferation but it is not a cell cycle-regulated gen
e. Finally, we studied thymosin beta 4 mRNA stability by inhibiting th
ymosin beta 4 gene transcription with actinomycin D. Our results sugge
st that thymosin beta 4 mRNA has a pronounced stability, a fact that m
ight be relevant to account for the presence of thymosin beta 4 in enu
cleated cells like platelets.