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Published February 24, 1989 | public
Journal Article

Reciprocal effects of hyper- and hypoactivity mutations in the Drosophila pattern gene torso


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.

Additional Information

© 1989 American Association for the Advancement of Science. 29 August 1988; Accepted 29 November 1988. We thank T. Schüpbach for providing the tor^(splc) allele, for communicating unpublished data, and for helpful discussions. We thank E. B. Lewis for providing Dp(2;3)P32, M. Ashburner for Df(2R)CA58, and J. Topol, C. Dearolf, and C. Parker for providing the ftz-β-gal EΔ-669 transformed line. P. Sternberg, S. Lewis, and D. Mathog provided critical comments on the manuscript. T.R.S. is supported by a junior postdoctoral fellowship from the American Cancer Society (California Division), S.R.H. by a predoctoral traineeship from the NIH, USPHS GM07616. This research was funded by USPHS research grant HD23099 to H.D.L.

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