Abstract
By screening for mutations that suppress the vulval defects caused by a constitutively active let-60 ras gene, we identified six loss-of-function alleles of ksr-1, a novel C. elegans gene. Our genetic analysis showed ksr-1 positively mediates Ras signaling and functions downstream of or in parallel to let-60. In the absence of ksr-1 function, normal Ras signaling is impaired only slightly, suggesting ksr-1 may act to modulate, or in a branch that diverges from, the main signaling pathway. The predicted KSR-1 protein has a protein kinase domain and is most similar to a recently identified Drosophila protein involved in Ras signaling. We propose that the function of ksr-1 is evolutionarily conserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Base Sequence
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Caenorhabditis elegans / embryology
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Caenorhabditis elegans / enzymology
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Caenorhabditis elegans / genetics*
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Caenorhabditis elegans Proteins*
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Chromosome Mapping
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Cloning, Molecular
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Embryonic Induction
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Female
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Genes, Helminth / genetics*
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Genes, Suppressor / genetics
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Helminth Proteins / genetics
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Molecular Sequence Data
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Mutation
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Protein Kinases / chemistry
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Protein Kinases / genetics*
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Protein Kinases / physiology
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RNA, Helminth / analysis
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RNA, Messenger / analysis
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Sequence Analysis, DNA
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Sequence Homology, Amino Acid
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Signal Transduction / physiology*
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Vulva / embryology
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ras Proteins / physiology*
Substances
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Caenorhabditis elegans Proteins
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Helminth Proteins
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RNA, Helminth
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RNA, Messenger
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let-60 protein, C elegans
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Protein Kinases
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KSR-1 protein kinase
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ras Proteins