Because ribosome biogenesis plays an essential role in cell proliferation,
control mechanisms may have evolved to recognize Lesions in this critical a
nabolic process. To test this possibility, we conditionally deleted the gen
e encoding 40S ribosomal protein S6 in the Liver of adult mice. Unexpectedl
y, Livers from fasted animals deficient in S6 grew in response to nutrients
even though biogenesis of 40S ribosomes was abolished. However, Liver cell
s failed to proliferate or induce cyclin E expression after partial hepatec
tomy, despite formation of active cyclin D-CDK4 complexes. These results im
ply that abrogation of 40S ribosome biogenesis may induce a checkpoint cont
rol that prevents cell cycle progression.