We have transiently expressed a dominant negative form of rad (N17rac1
) using adenoviral-mediated gene transfer. The level of N17rac1 expres
sion is demonstrated to be proportional to the multiplicity of infecti
on. Expression of N17rac1 in Rat 2 fibroblasts results in cytostatic g
rowth arrest. Cell-cycle analysis demonstrates that cells expressing N
17rac1 accumulate in G2/M. These results suggest that rad is required
for cell proliferation and provide the first demonstration in mammalia
n cells of a role for small GTP-binding proteins in the G2/M transitio
n.