Mutant flies have a mild ectopic vein phenotype in the wing.
germline clones result in embryonic lethality characterized by moderate head defects in 80% of clonal embryos. The embryos also display moderate and variable segmentation defects, including loss of denticle structures. They also show a reduction in embryonic cell death, particularly in the head region. Post death stage homozygous nmoadk1
pupal retinae have an increased density of secondary/tertiary pigment cells compared to wild-type. Unlike wild-type, the local density of these cells is variable: dependent on the specific aberrations in ommatidial shape and orientation in the region in question. In some regions the ommatidia are square-like and have approximately wild-type numbers of secondary/tertiary cells. In other regions of the same retina, ommatidia retain a hexagonal- like shape but have increased numbers of secondary/tertiary pigment cells.
Mutant flies have a shorter, broader wing than normal. Excess wing vein tissue originating from the posterior crossvein and extending distally between veins L4 and L5 is seen (this phenotype is fully penetrant). Additional vein material can also form parallel to vein L2 and posterior to vein L5. The wings are held away from the body at a 45o angle. Flies show a variable polarity defect in the wing. Homozygotes show a mild loss of bristles on the head and notum (having an average of 37.4 +/- 1.71 bristles compared to the wild-type number of 40) and occasionally have bent or duplicated bristles.
Semi-lethal, rare homozygous flies display rough, small eyes and several wing phenotypes. Wings are rounder and shorter and held out at an angle from the body, and also display ectopic cross vein material.