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Science 2 May 1997:
Vol. 276. no. 5313, pp. 791 - 794
DOI: 10.1126/science.276.5313.791

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 dagger

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.

dagger    To whom correspondence should be addressed. E-mail: abernards{at}helix.mgh.harvard.edu


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