👤 A García-Bellido

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. Show less

Contrabithorax (Cbx) alleles are dominant mutations in the Ultrabithorax (Ubx) gene of Drosophila that cause its ectopic expression in the mesothorax. We have studied the role of the homologous chromosome in the mesothoracic phenotype in several Cbx heterozygotes. None of the Cbx alleles studied shows variations in phenotype with extra doses of the Ubx gene. Only Cbx2 and CbxIRM (a revertant of Cbx1) show synapsis-dependent gene expression ("transvection"). The mesothoracic phenotypes of CbxIRM and Cbx2 heterozygotes are strongly modified when the homologous chromosome carries breakpoints proximal to or at the Ubx locus or null alleles of this gene. These lesions in the homologous chromosome enhance the Cbx2 mutant phenotype and reduce that of CbxIRM one. The genetic analysis of these transvection effects suggests that the transcription of the CbxIRM and Cbx2 alleles depends on RNAs of short radius of action from the homologous Ubx gene. Show less