Abstract
A screen for synthetic enhancers of sli-1 identified ark-1 (forAck-related tyrosine kinase), a novel inhibitor of let-23 EGFR signaling in C. elegans. An ark-1 mutation synergizes with mutations in other negative regulators of let-23, resulting in increased RAS signaling. Genetic analysis suggests that ARK-1 acts upstream of RAS and is dependent upon SEM-5. ARK-1 inhibits LET-23-mediated ovulation, a RAS-independent function. ARK-1 physically interacts with SEM-5 in the yeast two-hybrid assay. We find that sem-5 also has a negative function in let-23-mediated ovulation and suggest that this negative function is mediated by the recruitment of inhibitors such as ARK-1.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Caenorhabditis elegans / genetics
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Caenorhabditis elegans / growth & development
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Caenorhabditis elegans / metabolism*
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Caenorhabditis elegans Proteins*
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Cloning, Molecular
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ErbB Receptors / metabolism*
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Female
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Fertility / physiology
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Genes, Helminth
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Genes, Lethal
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Genes, ras
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Helminth Proteins / metabolism*
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Models, Biological
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Molecular Sequence Data
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Mutation
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Ovulation / physiology
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Protein-Tyrosine Kinases / genetics
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Protein-Tyrosine Kinases / metabolism*
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Sequence Homology, Amino Acid
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Signal Transduction
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Two-Hybrid System Techniques
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Vulva / growth & development
Substances
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Caenorhabditis elegans Proteins
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Helminth Proteins
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Ack-related tyrosine kinase-1, C elegans
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ErbB Receptors
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Protein-Tyrosine Kinases
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let-23 protein, C elegans