R cell MARCM clones of stan loss of function alleles are indistinguishable from control axons throughout their trajectory and invariably choose appropriate postsynaptic targets. Non-cell autonomous inappropriate axon targeting of wildtype R1, R4, R5 and R6 cells is seen when in the presence of stan mutant neighbours. In single-cell clones in which the wildtype cells targeted normally, directly neighbouring cells and those separated by a single cell are mutant with approximately equal frequency, whilst those separated by two intervening cells are mutant approximately half as often. In cases where the wildtype cell mistargeted, 12/14 clones have a single mutant immediate-neighbour, 2/14 have a single mutant neighbour with an intervening cell, and no cases have a mutant cell separated by two intervening cells. Pooling this data with the data from all clones, including those with multiple wildtype axons and multiple mutant cells: 77% of wildtype clones that mistarget have an abutting mutant cell; 11% have a mutant cell separated by either one or two intervening cells; and 11% have only mutant neighbours in an adjacent ommatidium.

17% of wildtype cells directly adjacent to a stan mutant cell target inappropriately. 4% of wildtype cells separated from a mutant cell by one or two intervening cells, and 1.5% of axons with mutants in adjacent ommatidia target inappropriately.

In contrast to wild-types, wing membrane ridges appear disrupted in a stan^unspecified mutant.

Mutant ES neurons in the dorsal cluster have pathfinding defects and terminate in ectopic locations.

Mutants show no gross defects in anterior-posterior or dorsal-ventral patterning.

Show no interaction with the dominant wing basal cell 1 swirl phenotype of Vang^Tbs42.