Contrabithorax mutations cause inappropriate expression of Ultrabithorax products in Drosophila

Abstract

The mutation Contrabithorax (Cbx) has played an important part in the recognition of the role that genes of the bithorax complex (BX-C) play in the control of development. Contrabithorax, a dominant mutation which maps in the proximal or Ultrabithorax domain of the BX-C, results in the transformation of structures of the second thoracic segment (T2) into homologous structures of T3 (ref. 1). Recessive mutations and deletions of the same chromosome region have the reverse effect, transforming T3 into T2. This reciprocal relationship between the effects of dominant (gain of function) and recessive (loss of function) mutations suggested that products of the BX-C were both necessary and sufficient to specify the unique developmental pathways of different segments². Here we report that the original Contrabithorax mutation (Cbx¹) and two other dominant mutations in the Ultrabithorax domain, Cbx³ (ref. 3) and Haltere mimic (Hm)^3,4, all cause the inappropriate expression in T2 of products from the Ultrabithorax (Ubx) trascription unit. This strongly supports the suggestion that these products execute the functions of the proximal or Ultra-bithorax domain of the BX-C⁵.