Rac1 is required for cell proliferation and G2/M progression.
We have transiently expressed a dominant negative form of rac1 (N17rac1) using adenoviral-mediated gene transfer. The level of N17rac1 expression is demonstrated to be proportional to the multiplicity of infection. Expression of N17rac1 in Rat 2 fibroblasts results in cytostatic growth arrest. Cell-cycle analysis demonstrates that cells expressing N17rac1 accumulate in G2/M. These results suggest that rac1 is required for cell proliferation and provide the first demonstration in mammalian cells of a role for small GTP-binding proteins in the G2/M transition.
Moore
K A
KA
Cardiology Branch, National Heart, Lung and Blood Institute, Bethesda, MD 20892-1650, USA.
Sethi
R
R
Doanes
A M
AM
Johnson
T M
TM
Pracyk
J B
JB
Kirby
M
M
Irani
K
K
Goldschmidt-Clermont
P J
PJ
Finkel
T
T
D000256:Adenoviridae / Q000235:genetics; D000818:Animals; D015153:Blotting, Western; D002455:Cell Division / Q000187:drug effects / Q000235:genetics; D002460:Cell Line; D005347:Fibroblasts; D016195:G2 Phase / Q000187:drug effects / Q000235:genetics; D019204:GTP-Binding Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D018014:Gene Transfer Techniques; D008938:Mitosis / Q000187:drug effects / Q000235:genetics; D051381:Rats; D020744:rac GTP-Binding Proteins
D019204:GTP-Binding Proteins; D020744:rac GTP-Binding Proteins