Homoeosis in Drosophila: the ultrabithorax larval syndrome.

Abstract

Recent results [Morata, G. & Kerridge, S. (1981) Nature (London) 290, 778-781] have shown that early Ultrabithorax- clones transform the posterior compartments of the adult meso- and metathoracic legs to prothorax. These transformations have not been seen in Ultrabithorax homozygous larvae, which are reported to show only transformations of the metathorax and the first abdominal segment to mesothorax [Lewis, E. B. (1978) Nature (London) 276, 565-570]. However, as the ventral surface of the larva does not exhibit sufficient markers to distinguish the posterior regions of these segments, cryptic larval transformations similar to those in the adult have been suggested (by Morata and Kerridge). We have further examined larvae of wild-type and various Ultrabithorax mutant genotypes, with particular attention to the dorsal surface. We find that Ultrabithorax homozygous larvae exhibit dorsal abnormalities consistent with transformations of the anterior metathorax and anterior first abdominal segment to mesothorax and of the posterior meso- and metathorax to prothorax as predicted by Morata and Kerridge; however, the posterior of the first abdominal segment remains untransformed. We suggest that in both larvae and adults the posterior first abdominal segment remains untransformed by Ultrabithorax mutations and that the unit of development with regard to the proximal bithorax complex consists of adjoining posterior and anterior compartments from neighboring segments rather than of segments themselves.

Trans regulation in the Ultrabithorax gene of Drosophila: alterations in the promoter enhance transvection.

“…Both alleles, UbxJ95rxJ and UbxMX6, are homozygous and hemizygous lethal. UhxJ95rxl mutant embryos show the characteristic syndrome described for Ubx null alleles (Lewis, 1978;Hayes et al, 1984); parasegments 5 and 6 are transformed into parasegment 4 and there is a slight thoracic transformation of the A2 -A7 abdominal segments.…”

Mutations in the Drosophila gene extradenticle affect the way specific homeo domain proteins regulate segmental identity.

“…Some double and triple mutant combinations are illustrated in Figure 3, and the rest are summarized in Table 1. Although homeotic genes act in parasegmental patterns (Hayes et al 1984;Struhl 1984), we will discuss mutant phenotypes in terms of segments, which are easier to visualize. In addition, because exd mutations cause one wild-type segment to look like another, we will distinguish between the position of a segment on the embryonic body (e.g., "AI"), and the cuticular structures found in a given segment of a wild-type embryo (e.g., the "A1 morphology").…”

Enhancer of Polycomb1, a Novel Homeodomain Only Protein-binding Partner, Induces Skeletal Muscle Differentiation

“…Although homozygotic mutations of E(Pc) in Drosophila are lethal in the embryo, heterozygous mutations do not by themselves result in a zygotic homeotic phenotype. Rather, mutations in E(Pc) enhance the phenotypes in mutations of other PcG genes (3,4). Although Epc1 itself does not have enzymatic activity, the complex, including Epc1, is reported to possess both activating and repressive activities as a transcription regulator.…”