Mevinolin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, w
as used to study the importance of mevalonic acid (MVA) for cell cycle
progression of tobacco (Nicotiana tabacom L.) BY-2 cells. After treat
ment with 5 mu M mevinolin, the cell cycle progression was completely
blocked and two cell populations accumulated (80% in phase G0/G1 and 2
0% in G2/M). The arrest could be released by subsequent addition of MV
A. Effects were compared to those caused by aphidicolin, an inhibitor
of alpha-like DNA polymerases that blocks cell cycle at the entry of t
he S phase. The 80% proportion of mevinolin-treated TBY-2 cells was cl
early arrested before the aphidicolin-inducible block. By the aid of a
double-blocking technique, it was shown that the mevinolin-induced ce
ll arrest of highly synchronized cells was due to interaction with a c
ontrol point located at the mitotic telophase/entry G1 phase. Dependin
g on the developmental stage, mevinolin induced rapid cell death in a
considerable percentage of cells. Mevinolin treatment led to a partial
synchronization, as shown by the increase in mitotic index. The follo
wing decrease was correlated with the above-mentioned induction of cel
l death.