The downregulation of the miniature gene does not replicate miniature loss-of-function phenotypes in Drosophila melanogaster wing to the full extent.

During maturation Drosophila wing epithelial cells undergo number of changes due to processes, which take place in the wing of the newly emerged fly, among which epithelial-to-mesenchymal transition (EMT) and apoptosis are pivotal. It is considered that neurohormone bursicon is responsible for their triggering. In turn, extracellular matrix protein Miniature is also essential for proper progress of apoptosis and, presumably, EMT. In accordance with our previously proposed hypothesis, Miniature and bursicon form stabilizing/accumulative complexes, which are able to diffuse freely within Drosophila wing, in such a way constitutively promoting enough concentrations of the maturation triggering signal. Here we tried to come to confirmation of our hypothesis from the other side, using UAS/GAL4 system and RNAi-silencing techniques.