Rescue of a Drosophila NF1 Mutant Phenotype by Protein Kinase A-Reference-Cited by-同舟云学术

Rescue of a Drosophila NF1 Mutant Phenotype by Protein Kinase A

Published:1997-05-02 Issue:5313 Volume:276 Page:791-794
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

The Inge¹²³,Hannigan Gregory E.¹²³,Cowley Glenn S.¹²³,Reginald Shoba¹²³,Zhong Yi¹²³,Gusella James F.¹²³,Hariharan Iswar K.¹²³,Bernards André¹²³

Affiliation:

1. 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.

2. 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.

3. Y. Zhong, Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.

Abstract

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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