TY - JOUR
T1 - The Drosophila abelson proto-oncogene homolog
T2 - Identification of mutant alleles that have pleiotropic effects late in development
AU - Henkemeyer, Mark J.
AU - Gertler, Frank B.
AU - Goodman, William
AU - Hoffmann, F. Michael
N1 - Funding Information:
We dedicate this research in memory of Christine A. Phelan. This work was begun by F M. H. in the laboratory of Dr. William Gelbart, whom we thank for his support and for providing facilities. We thank Drs. K. Loughney, T. Gilmore, H. Temin, and W. Dove for comments on the manuscript, and M. Belete, W. Russell, and Dr. C. Sattler for help with the eye sections. The work has been funded by American Cancer Society grant NP483 to F. M. H., Cancer Center Support NCI-CA07175 to
PY - 1987/12/4
Y1 - 1987/12/4
N2 - The Abelson gene in Drosophila (abl) consists of ten exons extending over 26 kb of genomic DNA. The DNA sequence encodes a protein of 1520 amino acids with sequence homology to the human c-abl proto-oncogene product, beginning at the amino terminus and extending 656 amino acids through the region essential for tyrosine kinase activity. Mutant lesions in the abl gene were identified first by their failure to complement chromosomal deletions that overlap the abl DNA sequence and then by rescue of the mutant phenotypes with an abl minigene in transgenic flies. Elimination of abl zygotic function by mutations produces some recessive lethality at the pharate adult pupal stage, and mutant adults with reduced longevity, reduced fecundity, and an irregular pattern of retinal cells.
AB - The Abelson gene in Drosophila (abl) consists of ten exons extending over 26 kb of genomic DNA. The DNA sequence encodes a protein of 1520 amino acids with sequence homology to the human c-abl proto-oncogene product, beginning at the amino terminus and extending 656 amino acids through the region essential for tyrosine kinase activity. Mutant lesions in the abl gene were identified first by their failure to complement chromosomal deletions that overlap the abl DNA sequence and then by rescue of the mutant phenotypes with an abl minigene in transgenic flies. Elimination of abl zygotic function by mutations produces some recessive lethality at the pharate adult pupal stage, and mutant adults with reduced longevity, reduced fecundity, and an irregular pattern of retinal cells.
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U2 - 10.1016/0092-8674(87)90105-X
DO - 10.1016/0092-8674(87)90105-X
M3 - Article
C2 - 3119227
AN - SCOPUS:0023644225
SN - 0092-8674
VL - 51
SP - 821
EP - 828
JO - Cell
JF - Cell
IS - 5
ER -