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Science 2 May 1997: Vol. 276. no. 5313, pp. 791 - 794 DOI: 10.1126/science.276.5313.791
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Reports
Rescue of a Drosophila NF1 Mutant Phenotype by Protein Kinase A
Inge The,
Gregory E. Hannigan,
*
Glenn S. Cowley,
Shoba Reginald,
Yi Zhong,
James F. Gusella,
Iswar K. Hariharan,
André Bernards
The neurofibromatosis type 1 (NF1) tumor suppressor protein is
thought to restrict cell proliferation by functioning as a Ras-specific
guanosine triphosphatase-activating protein. However, Drosophila homozygous for null mutations of an
NF1 homolog showed no obvious signs of perturbed
Ras1-mediated signaling. Loss of NF1 resulted in a reduction
in size of larvae, pupae, and adults. This size defect was not modified
by manipulating Ras1 signaling but was restored by expression of
activated 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.
I. The, G. S. Cowley, S. Reginald, I. K. Hariharan, A. Bernards,
Massachusetts General Hospital Cancer Center and Harvard Medical School
Building 149, 13th Street, Charlestown, MA 02129, USA.
G. E. Hannigan and J. F. Gusella, Molecular Neurogenetics Unit,
Massachusetts General Hospital and Harvard Medical School Building 149, 13th Street, Charlestown, MA 02129, USA.
Y. Zhong, Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring
Harbor, NY 11724, USA.
*
Present address: Division of Pathology, The Hospital for Sick
Children, 555 University Avenue, Toronto M5G 1X8, Canada.
To whom correspondence should be addressed. E-mail:
abernards{at}helix.mgh.harvard.edu
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