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Science 24 February 1989:
Vol. 243. no. 4894, pp. 1062 - 1066
DOI: 10.1126/science.2922596
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Articles
Science, Vol 243, Issue 4894, 1062-1066
Copyright © 1989 by American Association for the Advancement of Science
Reciprocal effects of hyper- and hypoactivity mutations in the Drosophila pattern gene torso
TR Strecker,
Halsell SR,
WW Fisher,
and
HD Lipshitz
Division of Biology, California Institute of Technology, Pasadena 91125.
In Drosophila, five "terminal" polarity genes must be active in females in order for them to produce embryos with normal anterior and posterior ends. Hypoactivity mutations in one such gene, torso, result in the loss of the most posterior domain of fushi tarazu expression and the terminal cuticular structures. In contrast, a torso hyperactivity mutation causes the loss of central fushi tarazu expression and central cuticular structures. Cytoplasmic leakage, transplantation, and temperature-shift experiments suggest that the latter effect is caused by abnormal persistence of the torso product in the central region of the embryo during early development. Thus, the amount and timing of torso activity is key to distinguishing the central and terminal regions of the embryo. Mutations in the tailless terminal gene act as dominant maternal suppressors of the hyperactive torso allele, indicating that the torso product acts through, or in concert with, the tailless product.
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