Abstract
Dorsal-ventral axis formation in the Drosophila wing depends on the activity of the LIM homeodomain transcription factor Apterous and its cofactor, dLDB/Chip. We present evidence that Apterous activity depends on the formation of a LIM homeodomain dimer bridged by a dimer of cofactor. We show that Apterous activity levels are regulated in vivo by dLMO, an antagonist of homodimer formation. Making use of a constitutively active form of Apterous and dominant-negative forms of Apterous and dLDB/Chip, we show that the normal function of dLMO is to downregulate Apterous activity and that the dLMO mutant phenotype is due to excess Apterous activity. These findings may point to a general mechanism for regulation of LIM homeodomain protein activity.
MeSH terms
-
Animals
-
Body Patterning
-
Cloning, Molecular
-
Dimerization
-
Drosophila / genetics*
-
Drosophila / growth & development*
-
Drosophila Proteins*
-
Homeodomain Proteins / genetics
-
Homeodomain Proteins / metabolism*
-
Insect Proteins / metabolism
-
LIM-Homeodomain Proteins
-
Macromolecular Substances
-
Nuclear Proteins / chemistry
-
Nuclear Proteins / genetics
-
Nuclear Proteins / metabolism*
-
Polymerase Chain Reaction
-
Recombinant Proteins / metabolism
-
Transcription Factors / chemistry
-
Transcription Factors / genetics
-
Transcription Factors / metabolism*
-
Wings, Animal / growth & development*
Substances
-
Bx protein, Drosophila
-
Chi protein, Drosophila
-
Drosophila Proteins
-
Homeodomain Proteins
-
Insect Proteins
-
LIM-Homeodomain Proteins
-
Macromolecular Substances
-
Nuclear Proteins
-
Recombinant Proteins
-
Transcription Factors
-
ap protein, Drosophila