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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2005-10-3
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pubmed:abstractText |
lin-1 encodes an ETS domain transcription factor that functions downstream of a Ras/MAP kinase pathway mediating induction of the 1 degrees cell fate during vulval development in the C. elegans hermaphrodite. Mutants lacking lin-1 activity display a phenotype similar to that caused by mutations that constitutively activate let-60 Ras consistent with a model in which lin-1 is a repressor of the 1 degree fate whose activity is inhibited by phosphorylation by MPK-1 MAP kinase. Here, we show that, contrary the current model, lin-1 is required positively for the proper expression of several genes regulated by the pathway in cells adopting the 1 degrees cell fate. We show that the positive requirement for lin-1 is downstream of let-60 Ras and mpk-1 MAP kinase, and that it has a focus in the vulval precursor cells themselves. lin-1 alleles encoding proteins lacking a docking site for MPK-1 MAP kinase are defective in the positive function. We also show that lin-1 apparently has both positive and negative functions during the specification of the fates of other cells in the worm requiring Ras/MAP kinase signaling.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caenorhabditis elegans Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Egl-17 protein, C elegans,
http://linkedlifedata.com/resource/pubmed/chemical/Green Fluorescent Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Lin-1 protein, C elegans,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/let-60 protein, C elegans,
http://linkedlifedata.com/resource/pubmed/chemical/lin-31 protein, C elegans,
http://linkedlifedata.com/resource/pubmed/chemical/mpk-1 protein, C elegans,
http://linkedlifedata.com/resource/pubmed/chemical/ras Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0012-1606
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
286
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
338-51
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:16140291-Animals,
pubmed-meshheading:16140291-Animals, Genetically Modified,
pubmed-meshheading:16140291-Caenorhabditis elegans,
pubmed-meshheading:16140291-Caenorhabditis elegans Proteins,
pubmed-meshheading:16140291-DNA-Binding Proteins,
pubmed-meshheading:16140291-Disorders of Sex Development,
pubmed-meshheading:16140291-Female,
pubmed-meshheading:16140291-Gene Expression Regulation, Developmental,
pubmed-meshheading:16140291-Genes, Helminth,
pubmed-meshheading:16140291-Green Fluorescent Proteins,
pubmed-meshheading:16140291-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:16140291-MAP Kinase Signaling System,
pubmed-meshheading:16140291-Male,
pubmed-meshheading:16140291-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:16140291-Mutation,
pubmed-meshheading:16140291-Protein-Serine-Threonine Kinases,
pubmed-meshheading:16140291-Recombinant Proteins,
pubmed-meshheading:16140291-Transcription Factors,
pubmed-meshheading:16140291-Vulva,
pubmed-meshheading:16140291-ras Proteins
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pubmed:year |
2005
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pubmed:articleTitle |
lin-1 has both positive and negative functions in specifying multiple cell fates induced by Ras/MAP kinase signaling in C. elegans.
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pubmed:affiliation |
Umeå Center for Molecular Pathogenesis, Umeå University, SE-901 87 Umeå, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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