Cell cycle-dependent inhibition of p34cdc2 synthesis by transforming growth factor beta 1 in cycling epithelial cells.
Cycling epithelial cells were shown to reversibly arrest in late G1 phase following treatment with transforming growth factor beta 1. Associated with this G1-S phase arrest was a decrease in the synthesis and histone H1 kinase activity of p34cdc2. Transforming growth factor beta 1 did not reduce p34cdc2 levels by modulating the turnover of newly synthesized p34cdc2. The decrease in p34cdc2 synthesis preceded any detectable effect on DNA synthesis. Moreover, the action of transforming growth factor beta 1 was regulated in a cell cycle-specific manner; epithelial cells were sensitive to transforming growth factor beta 1 only during the G1 phase. The results suggest that p34cdc2 might be a useful biochemical marker for investigating the mechanism(s) of transforming growth factor beta 1 signaling.
Eblen
S T
ST
Department of Cell Biology, Vanderbilt University, Nashville, Tennessee 37232.
Fautsch
M P
MP
Burnette
R J
RJ
Joshi
P
P
Leof
E B
EB
D000818:Animals; D016203:CDC2 Protein Kinase / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D002453:Cell Cycle / Q000187:drug effects / Q000502:physiology*; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D016895:Culture Media, Serum-Free; D004847:Epithelial Cells; D004848:Epithelium / Q000187:drug effects / Q000201:enzymology; D016193:G1 Phase; D007700:Kinetics; D008168:Lung; D008907:Mink; D016196:S Phase; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000494:pharmacology*
D016895:Culture Media, Serum-Free; D016212:Transforming Growth Factor beta; D016203:CDC2 Protein Kinase