A dose-sensitive modifier of the of Drosophila melanogaster ectopic eye

Ectopic eyes induced in a wing serve as a system for studying developmental plasticity in Drosophila. We used a set of chromosome deficiencies covering the second chromosome to ask whether there are dose-sensitive modifiers of the process. We identified three overlapping deletions showing the enlargement of ectopic eyes. The study of the genes localized in the region of interest suggests that the mutation in the sxc (super sex combs) gene (PcG group) is responsible for the observed phenotype.

The Drosophila homeobox gene optix is capable of inducing ectopic eyes by an eyeless-independent mechanism

optix is a new member of the Six/so gene family from Drosophila that contains both a six domain and a homeodomain. Because of its high amino acid sequence similarity with the mouse Six3 gene, optix is considered to be the orthologous gene from Drosophila rather than sine oculis, as previously believed. optix expression was detected in the eye, wing and haltere imaginal discs. Ectopic expression of optix leads to the formation of ectopic eyes suggesting that optix has important functions in eye development. Although optix and sine oculis belong to the same gene family (Six/so) and share a high degree of amino acid sequence identity, there are a number of factors which suggest that their developmental roles are different: (1) the expression patterns of optix and sine oculis are clearly distinct; (2) sine oculis acts downstream of eyeless, whereas optix is expressed independently of eyeless; (3) sine oculis functions synergistically with eyes absent in eye development whereas optix does not; (4) ectopic expression of optix alone, but not of sine oculis can induce ectopic eyes in the antennal disc. These results suggest that optix is involved in eye morphogenesis by an eyeless-independent mechanism.

Pax6 induces ectopic eyes in a vertebrate

We report here that misexpression of the transcription factor Pax6 in the vertebrate Xenopus laevis leads to the formation of differentiated ectopic eyes. Multiple molecular markers indicated the presence of mature lens fiber cells, ganglion cells, Muller cells, photoreceptors and retinal pigment epithelial cells in a spatial arrangement similar to that of endogenous eyes. Lineage tracing experiments showed that lens, retina and retinal pigment epithelium arose as a consequence of the cell-autonomous function of Pax6. These experiments also reveal that the cell autonomous activity of misexpressed Pax6 causes the ectopic expression of a number of genes including Rx, Otx2, Six3 and endogenous Pax6, each of which has been implicated in eye development. The formation of ectopic and endogenous eyes could be suppressed by coexpression of a dominant-negative form of Pax6. These data show that in vertebrates, as in the invertebrate Drosophila melanogaster, Pax6 is both necessary and sufficient to trigger the cascade of events required for eye formation.

Control of Drosophila adult pattern by extradenticle

The homeobox gene extradenticle (exd) acts as a cofactor of the homeotic genes in the specification of larval patterns during embryogenesis. To study its role in adult patterns, we have generated clones of mutant exd- cells and examined their effect on the different body parts. In some regions, exd- clones exhibit homeotic transformations similar to those produced by known homeotic mutations such as Ultrabithorax (Ubx), labial (lab), spineless-aristapedia (ssa) or Antennapedia (Antp). In other regions, the lack of exd causes novel homeotic transformations producing ectopic eyes and legs. Moreover, exd is also required for functions normally not associated with homeosis, such as the maintenance of the dorsoventral pattern, the specification of subpatterns in adult appendages or the arrangement of bristles in the mesonotum and genitalia. Our findings indicate that exd is critically involved in adult morphogenesis, not only in the homeotic function but also in several other developmental processes.

ON THE DEVELOPMENT OF ECTOPIC EYES IN DROSOPHILA MELANOGASTER PRODUCED BY THE MUTATION EXTRA EYE (EE)

ABSTRACT The mutation ee often produces an ectopic eye on the vertex that is a mirror image partial duplication of the normal eye on the ipsilateral side of the head. The pattern of the duplication and a clonal analysis by mitotic recombination indicate that the duplications are of dorsal eye and orbital structures. Large ectopic eyes (more than 100 ommatidia) and their surrounding bristles may be produced without cuticular deficiencies. The penetrance of ee is temperature dependent with penetrance higher (72%) at 25° and 29° than at 19° (43%). Temperature shift experiments show two temperature-sensitive periods: one at midembryogenesis, the other at mid-first larval instar. Microscopic examination of ee late-second and third instar imaginal cephalic discs show no indication of growth of the extra tissue needed to produce the duplication until after mid-third instar. This was confirmed by cell counts of ee and wild-type discs. There is no evidence of differential cell death in the two types of discs at this stage, although much earlier cell death is postulated. Tests for cell autonomy of the mutation by the production of morphogenetic clones suggest nonautonomy. Formation of pattern duplications by mutant genes is discussed in terms of cell death that eliminates whole developmental compartments, restricted cell death that occurs within a compartment, extensive cell death within a compartment and proliferative growth unassociated with cell lethality.