Abstract
Wnt/Wingless directs many cell fates during development. Wnt/Wingless signaling increases the amount of beta-catenin/Armadillo, which in turn activates gene transcription. Here the Drosophila protein D-Axin was shown to interact with Armadillo and D-APC. Mutation of d-axin resulted in the accumulation of cytoplasmic Armadillo and one of the Wingless target gene products, Distal-less. Ectopic expression of d-axin inhibited Wingless signaling. Hence, D-Axin negatively regulates Wingless signaling by down-regulating the level of Armadillo. These results establish the importance of the Axin family of proteins in Wnt/Wingless signaling in Drosophila.
MeSH Terms
Adaptor Proteins, Signal Transducing
Adenomatous Polyposis Coli Protein
Animals
Armadillo Domain Proteins
Axin Protein
Body Patterning
Carrier Proteins/chemistry,genetics,metabolism
Chromosome Mapping
Cytoplasm/metabolism
Cytoskeletal Proteins/metabolism
Down-Regulation
Drosophila/embryology,genetics,metabolism
Drosophila Proteins
Embryo, Nonmammalian/metabolism
Extremities/embryology
Gene Expression Regulation, Developmental
Genes, Insect
Homeodomain Proteins/genetics,metabolism
In Situ Hybridization
Insect Proteins/genetics,metabolism
Molecular Sequence Data
Mutation
Phenotype
Proteins/chemistry,genetics,metabolism
Proto-Oncogene Proteins/metabolism
Recombinant Fusion Proteins/metabolism
Repressor Proteins
Signal Transduction
Trans-Activators
Transcription Factors
Wings, Animal/embryology,metabolism
Wnt1 Protein
Chemicals
APC protein, Drosophila
ARM protein, Drosophila
Adaptor Proteins, Signal Transducing
Adenomatous Polyposis Coli Protein
Armadillo Domain Proteins
Axin Protein
Axn protein, Drosophila
Carrier Proteins
Cytoskeletal Proteins
Drosophila Proteins
Homeodomain Proteins
Insect Proteins
Proteins
Proto-Oncogene Proteins
Recombinant Fusion Proteins
Repressor Proteins
Trans-Activators
Transcription Factors
Wnt1 Protein
distal-less protein, insect
wg protein, Drosophila
Authors & Affiliations
11 authors, click to expand affiliations / ORCID
Hamada F
Department of Oncogene Research, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita 565-0871, Japan.
Tomoyasu Y
Takatsu Y
Nakamura M
Nagai S
Suzuki A
Fujita F
Shibuya H
Toyoshima K
Ueno N
Akiyama T