Abstract
We have isolated mutations in the gene encoding a Drosophila 14-3-3 epsilon protein as suppressors of the rough eye phenotype caused by the ectopic expression of RAS1(V12). Using a simple loss-of-function 14-3-3 epsilon mutation, we show that 14-3-3 epsilon acts to increase the efficiency of RAS1 signaling. The 14-3-3 epsilon protein appears to function in multiple RTK pathways, suggesting that it is a general component of RAS1 signaling cascade. Sequence analysis of three dominant-negative alleles defines two regions of 14-3-3 epsilon that participate in RAS1 signaling. We also present evidence that 14-3-3 epsilon and 14-3-3 zeta, two 14-3-3 protein family members, are partially redundant for RAS1 signaling in photoreceptor formation and in animal viability. Our genetic data suggest that 14-3-3 epsilon functions downstream of or parallel to RAF, but upstream of nuclear factors in RAS1 signaling.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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14-3-3 Proteins
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Alleles
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Amino Acid Sequence
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Animals
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Drosophila / anatomy & histology
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Drosophila / genetics
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Drosophila / physiology*
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Eye / anatomy & histology
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Genes, Insect
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Microscopy, Electron, Scanning
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Models, Molecular
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Molecular Sequence Data
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Mutation
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Phenotype
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / physiology
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Proteins / chemistry
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Proteins / genetics
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Proteins / physiology*
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / physiology
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Proto-Oncogene Proteins c-raf
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Sequence Homology, Amino Acid
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Signal Transduction
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Suppression, Genetic
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Tyrosine 3-Monooxygenase*
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ras Proteins / genetics
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ras Proteins / physiology*
Substances
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14-3-3 Proteins
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Proteins
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Proto-Oncogene Proteins
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Tyrosine 3-Monooxygenase
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-raf
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ras Proteins
Associated data
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GENBANK/U84897
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GENBANK/U84898