The neurofibromatosis type 1 (NF1) tumor suppressor protein is thought
to restrict cell proliferation by functioning as a Ras-specific guano
sine triphosphatase-activating protein. However, Drosophila homozygous
for null mutations of an NF1 homolog showed no obvious signs of pertu
rbed Ras1-mediated signaling, Loss of NF1 resulted in a reduction in s
ize of larvae, pupae, and adults. This size defect was not modified by
manipulating Ras1 signaling but was restored by expression of activat
ed adenosine 3',5'-monophosphate-dependent protein kinase (PKA). Thus,
NF1 and PKA appear to interact in a pathway that controls the overall
growth of Drosophila.