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Published February 1, 1990 | Published
Journal Article Open

Dosage requirements of Ultrabithorax and bithoraxoid in the determination of segment identity in Drosophila melanogaster

Abstract

The wild-type Ultrabithorax (Ubx) and bithoraxoid (bxd) functions are primarily responsible for establishing the identity of parasegment 6 (PS6) in the Drosophila embryo and thus the identity of the posterior compartment of the third thoracic segment (pT3) and the anterior compartment of the first abdominal segment (aA1) in the adult. The experiments described were designed to test the ability of an increased dosage of Ubx⁺ and bxd⁺ to affect the transformation of PS5 toward PS6. The results are consistent with the ideas that (1) multiple copies of Ubx⁺ and bxd⁺ cause some cells within PS5 to take on the characteristics of PS6 cells but do not cause an overall parasegmental transformation of PS5 toward PS6, (2) cellular identity depends not only on the activity of Ubx⁺ but on its concentration as well, and (3) that an interaction between Ubx⁺ and the wild-type Antennapedia (Antp) gene establishes segmental identity in pT2. In the first instar larvae carrying eight copies of Ubx⁺ and bxd⁺ the fine hairs of the T3 setal belt are transformed toward the hook-like structures of the A1 setal belt. Other structures within this segment are unaffected. In the adult, the haltere is reduced in size. The transformation of pT2 cells (wing) toward pT3 cells (haltere) is seen in adults carrying eight doses of wild type Ubx and bxd by decreasing the amount of the bithorax complex (BX-C) regulator Polycomb (Pc). However, the transformation of the T3 setal belt is not enhanced in the larvae of these animals. The interaction between the genes of the Antennapedia complex (ANT-C) and the Ubx⁺ and bxd⁺ functions in pT2 is dosage sensitive only when the animals carry one copy of Pc. In these animals, the transformation of wing toward haltere is significantly enhanced.

Additional Information

© 1990 by the Genetics Society of America. Manuscript received April 28, 1989; Accepted for publication November 4, 1989. I would like to thank E. B. LEWIS for advice and support while I completed this project. I would especially like to thank JIM POSAKONY, LEILA POSAKONY and WELCOME BENDER for helpful comments along the way. I am grateful to E. B. LEWIS, WELCOME BENDER and MICHAEL FORTE for a critical reading of the manuscript and to the reviewers for their thoughtful criticisms. This work was supported by a National Institutes of Health (NIH) fellowship (GM08984) and grants from the March of Dimes (No. 1-1029) and the NIH (No. HD06331) awarded to E. B. LEWIS. The publication costs of this article were partly defrayed by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. § 1734 solely to indicate this fact.

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August 19, 2023
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