THE neurofibromatosis 1 (NF1) gene product, neurofibromin, is a tumor
suppressor gene product capable of inhibiting the growth of cells in c
ulture. If neurofibromin suppresses cell growth by arresting cells in
G(0) or G(1), its expression might be regulated in a cell cycle-depend
ent fashion. In this study, we demonstrate that RAT-1A fibroblasts arr
ested in G(0)/G(1) by serum starvation and then released to progress t
hrough the cell cycle do not demonstrate significant changes in NF1 ex
pression. However, when arrested in G(0)/G(1) by contact inhibition, N
F1 expression in these cells is reversibly upregulated within 72 h, su
ggesting that NF1 expression is a late event associated with cell grow
th arrest which may contribute to the maintenance of the differentiate
d state.