We have studied the posterior spiracles of Drosophila as a model to link patterning genes and morphogenesis. A genetic cascade of transcription factors downstream of the Hox gene Abdominal-B subdivides the primordia of the posterior spiracles into two cell populations that develop using two different morphogenetic mechanisms. The inner cells that give rise to the spiracular chamber invaginate by elongating into "bottle-shaped" cells. The surrounding cells give rise to a protruding stigmatophore by changing their relative positions in a process similar to convergent extension. The genetic cascades regulating spiracular chamber, stigmatophore, and trachea morphogenesis are different but coordinated to form a functional tracheal system. In the posterior spiracle, this coordination involves the control of the initiation of cell invagination that starts in the cells closer to the trachea primordium and spreads posteriorly. As a result, the opening of the tracheal system shifts back from the spiracular branch of the trachea into the posterior spiracle cells. We analyze the contribution of the ems gene to this coordination. In ems mutants, invagination of the spiracle cells adjacent to the trachea does not occur, but more posterior cells of the spiracle invaginate normally. This results in a spiracle without a lumen and with the tracheal opening located outside it.

The activity of the Ultrabithorax gene is continuously required during imaginal development to maintain the morphogenetic identity of the third thoracic segment of Drosophila. The spatial pattern of Ultrabithorax gene expression depends on certain cis regulatory regions and several trans regulatory genes. Amongst the latter the Polycomb gene is necessary to maintain Ultrabithorax repressed in cells where it was not initially activated and the trithorax gene is required for maintaining the expression of the gene where initially active. We have studied genetic interactions between several Ultrabithorax mutations in coding and cis regulatory regions in combination with Polycomb and trithorax mutations. Our results suggest that Polycomb and trithorax gene products do not interact with Ultrabithorax protein products but interact (directly or indirectly) with specific and discrete cis regulatory regions such as those where anterobithorax and postbithorax but not bithorax mutations map. We discuss possible mechanisms of these interactions.

No abstract

In wild-type Drosophila melanogaster larvae, the Ultrabithorax (Ubx) gene is expressed in the haltere imaginal discs but not in the majority of cells of the wing imaginal discs. Ectopic expression of the Ubx gene in wing discs can be elicited by the presence of Contrabithorax (Cbx) gain-of-function alleles of the Ubx gene or by loss-of-function mutations in Polycomb (Pc) or in other trans-regulatory genes which behave as repressors of Ubx gene activity. Several Ubx loss-of-function alleles cause the absence of detectable Ubx proteins (UBX) or the presence of truncated UBX lacking the homeodomain. We have compared adult wing phenotypes with larval wing disc UBX patterns in genotypes involving double mutant chromosomes carrying in cis one of those Ubx mutations and the Cbx1 mutation. We show that such double mutant genes are (1) active in the same cells in which the single mutant Cbx1 is expressed, although they are unable to yield functional proteins, and (2) able to induce ectopic expression of a normal homologous Ubx allele in a part of the cells in which the single mutant Cbx1 is active. That induction is conditional upon pairing of the homologous chromosomes (the phenomenon known as transvection), and it is not mediated by UBX. Depletion of Pc gene products by Pc3 mutation strongly enhances the induction phenomenon, as shown by (1) the increase of the number of wing disc cells in which induction of the homologous allele is detectable, and (2) the induction of not only a paired normal allele but also an unpaired one.