@article {843026,
	title = {Drosophila wingless: a paradigm for the function and mechanism of Wnt signaling.},
	journal = {Bioessays},
	volume = {16},
	number = {6},
	year = {1994},
	month = {1994 Jun},
	pages = {395-404},
	abstract = {
	The link between oncogenesis and normal development is well illustrated by the study of the Wnt family of proteins. The first Wnt gene (int-1) was identified over a decade ago as a proto-oncogene, activated in response to proviral insertion of a mouse mammary tumor virus. Subsequently, the discovery that Drosophila wingless, a developmentally important gene, is homologous to int-1 supported the notion that int-1 may have a role in normal development. In the last few years it has been recognized that int-1 and Wingless belong to a large family of related glyco-proteins found in vertebrates and invertebrates. In recognition of this, members of this family have been renamed Wnts, an amalgam of int and Wingless. Investigation of Wnt genes in Xenopus and mouse indicates that Wnts have a role in cell proliferation, differentiation and body axis formation. Further analysis in Drosophila has revealed that Wingless function is required in several developmental processes in the embryo and imaginal discs. In addition, a genetic approach has identified some of the molecules required for the transmission and reception of the Wingless signal. We will review recent data which have contributed to our growing understanding of the function and mechanism of Drosophila Wingless signaling in cell fate determination, growth and specification of pattern.

},
	keywords = {Animals, Cell Differentiation, Cell Transformation, Neoplastic, Drosophila melanogaster, Drosophila Proteins, Embryonic Induction, Gene Expression Regulation, Metamorphosis, Biological, Mice, Morphogenesis, Multigene Family, Nervous System, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Proto-Oncogenes, Sequence Homology, Signal Transduction, Species Specificity, Wings, Animal, Wnt Proteins, Wnt1 Protein, Xenopus, Zebrafish Proteins},
	issn = {0265-9247},
	doi = {10.1002/bies.950160607},
	author = {Siegfried, E and Perrimon, N}
}
