Genetic interactions between the Drosophila Abelson (Abl) tyrosine kinase and failed axon connections (fax), a novel protein in axon bundles.
Mutations in the failed axon connections (fax) gene have been identified as dominant genetic enhancers of the Abl mutant phenotype. These mutations in fax all result in defective or absent protein product. In a genetic background with wild-type Abl function, the fax loss-of-function alleles are homozygous viable, demonstrating that fax is not an essential gene unless the animal is also mutant for Abl. The fax gene encodes a novel 47-kD protein expressed in a developmental pattern similar to that of Abl in the embryonic mesoderm and axons of the central nervous system. The conditional, extragenic noncomplementation between fax and another Abl modifier gene, disabled, reveal that the two proteins are likely to function together in a process downstream or parallel to the Abl protein tyrosine kinase.
Hill
K K
KK
McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison 53706, USA.
Bedian
V
V
Juang
J L
JL
Hoffmann
F M
FM
D000595:Amino Acid Sequence; D000818:Animals; D001369:Axons / Q000502:physiology*; D001483:Base Sequence; D015139:Blotting, Southern; D015153:Blotting, Western; D017931:DNA Primers; D029721:Drosophila Proteins; D004331:Drosophila melanogaster / Q000201:enzymology / Q000235:genetics* / Q000502:physiology; D005799:Genes, Dominant; D017344:Genes, Insect; D005804:Genes, Lethal; D005838:Genotype; D006579:Heterozygote; D008969:Molecular Sequence Data; D005810:Multigene Family; D016296:Mutagenesis; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000235:genetics*; D009424:Nervous System Physiological Phenomena; D016133:Polymerase Chain Reaction; D011505:Protein-Tyrosine Kinases / Q000235:genetics*; D016315:Proto-Oncogene Proteins c-abl / Q000235:genetics
D017931:DNA Primers; D029721:Drosophila Proteins; C097526:Fax protein, Drosophila; D009419:Nerve Tissue Proteins; D011505:Protein-Tyrosine Kinases; D016315:Proto-Oncogene Proteins c-abl