visible (with vriKG01220)
wing (with vriKG01220)
15% of stage 11-13 vri2/vrik05901 embryos show tracheal defects. During stages 14-17, 80% of vri2/vrik05901 embryos show weak tracheal defects (the general architecture of the trachea is preserved, but breaking of branches occurs and elongation and branching are abnormal) and 12% show strong tracheal defects (the tracheal architecture is strongly affected with complete disorganization and formation of sacs).
vriKG01220/vrik05901 flies have wings which are shorter than normal and which bend downwards, and the posterior scutellar bristles are upturned. Homozygous clones in the wing have pigmented regions that could result from necrosis. Clones at the anterior wing margin have smaller and thinner stout mechanosensory bristles than normal. The space between bristles is reduced, which is characteristic of smaller cells, and the margin is concave. The mean number of ommatidia in the eyes of mosaic flies in which the eyes are homozygous for vrik05901 is reduced by 10% compared to wild type.
The period length of the locomotor activity rhythm is significantly shorter in heterozygotes than in wild-type flies.
Homozygous embryo head skeleton is defective. In some embryos the germ band remains extended, suggesting defects in germ band retraction. Some embryos are convoluted, the ventral denticles extend laterally and filzkorper are internal and present an abnormal morphology. Hemizygotes die as larvae. A large number of undeveloped eggs are recovered from germline clones, phenotype can be rescued by paternal contribution of wild type vri.
Complements: cype03771. Complements: tkv04415. Complements: l(2)0488404884. Complements: l(2)k01302k01302. Complements: tkvk16713.
Mobilisation of the P{lacW} reveals the insertion is responsible for the mutant phenotype. 23 lethal revertant lines are selected and the lines that have a similar phenotype to vri1 and vri2 also die as larvae when hemizygous.