Nine X-ray-induced mutations of the bithorax complex (BX-C) have been isolated and characterized. They all show the typical features of the Ultrabithorax mutations. They are homozygous lethal, produce a slight enlargement of the haltere in heterozygous condition and fail to complement the mutations at the bx, bxd and pbx loci. Some of them are associated with chromosomal aberrations in the regions 89E 1-4, where the BX-C lies, while others appear normal cytologically.

The effect of six of these mutants in the adult cuticle has been studied, producing mutant marked clones in heterozygous individuals. The clones were generated by X-radiation at two points in development: the blastoderm stage and the second larval period. In all cases mutant clones showed the same phenotype: clones appearing in the dorsal structures transform metathorax and first abdominal segment towards mesothorax. That is the additive effect of bx, bxd and pbx mutations. Clones in the legs, if induced during the larval period, show an effect homologous to that seen in the dorsal structures. However, when produced at blastoderm they show in addition a transformation of the posterior second (mesothoracic) and third (metathoracic) legs into the posterior first (prothoracic) leg. This transformation, named postprothorax (ppx) has been recently described for the alleles Ubx130 and Ubx1 (Morata & Kerridge, 1981) and appears to be general for the Ubxmutations.

It is concluded that the realm of action of the Ubx gene is defined by part of the rflesothoracic segment (posterior second leg compartment) and the entire metathoracic and first abdominal segments.

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