Abstract
Dorso-ventral axis formation in the Drosophila wing requires the localized accumulation of the Apterous LIM/homeodomain protein (Ap) in dorsal cells. Here we report that dLdb/Chip encodes a LIM-binding cofactor that controls Ap activity. Both lack and excess of dLdb/Chip function cause the same phenotype as apterous (ap) lack of function; i.e. dorsal to ventral transformations, generation of new wing margins, and wing outgrowths. These results indicate that the normal function of Ap in dorso-ventral compartmentalization requires the correct amount of the DLDB/CHIP co-factor, and suggest that the Ap and DLDB/CHIP proteins form a multimeric functional complex. In support of this model, we show that the dLdb/Chip excess-of-function phenotypes can be rescued by ap overexpression.
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.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Animals, Genetically Modified
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Body Patterning
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Drosophila / growth & development
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Drosophila Proteins*
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Gene Expression
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Guinea Pigs
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Homeodomain Proteins / metabolism*
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Insect Proteins / genetics
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Insect Proteins / metabolism
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Insect Proteins / physiology*
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LIM-Homeodomain Proteins
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Mice
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Mosaicism
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Mutagenesis
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism
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Nuclear Proteins / physiology*
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Phenotype
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Transcription Factors / metabolism*
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Wings, Animal
Substances
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Chi protein, Drosophila
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Drosophila Proteins
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Homeodomain Proteins
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Insect Proteins
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LIM-Homeodomain Proteins
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Nuclear Proteins
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Transcription Factors
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ap protein, Drosophila