Rescue of the learning defect in dunce, a Drosophila learning mutant, by an allele of rutabaga, a second learning mutant
rutabaga1(rut1), a Drosophila learning mutant, has adenylate cyclase (EC 4.6.1.1) with reduced basal activity and the absence of calcium/calmodulin-stimulated activity. A second learning mutant, dunce, is defective in cyclic AMP degradation due to decreased or absent phosphodiesterase activity. Thes...
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Published in: | Proceedings of the National Academy of Sciences - PNAS Vol. 87; no. 7; pp. 2795 - 2799 |
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Main Author: | |
Format: | Journal Article |
Language: | English |
Published: |
Washington, DC
National Academy of Sciences of the United States of America
01-04-1990
National Acad Sciences |
Subjects: | |
Online Access: | Get full text |
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Summary: | rutabaga1(rut1), a Drosophila learning mutant, has adenylate cyclase (EC 4.6.1.1) with reduced basal activity and the absence of calcium/calmodulin-stimulated activity. A second learning mutant, dunce, is defective in cyclic AMP degradation due to decreased or absent phosphodiesterase activity. These opposing biochemical defects allow rut1to partially suppress the female sterility caused by elevated cyclic AMP levels in dunce flies. Selection of mutations that suppress dunce sterility has led to the isolation of two rutabaga alleles. The alleles (rut2and rut3) decrease basal adenylate cyclase activity [Bellen, H. J., Gregory, B. K., Olsson, C. L. \& Kiger, J. A. (1987) Dev. Biol. 121, 432-444] but, unlike the original rutabaga mutation, leave the calcium/calmodulin-stimulated activity intact. Behaviorally, the two alleles also differ from rut1. One of the mutations partially rescues the dunce learning defect, and flies bearing both alleles learn. Calcium responsiveness may thus be the crucial component of adenylate cyclase activity required for associative learning. |
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Bibliography: | 9035513 L50 L10 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0027-8424 1091-6490 |
DOI: | 10.1073/pnas.87.7.2795 |