rhoPΔ38 mutant clones generated in third instar larval eye discs occasionally show some morphological defects in the visual system, although lamina cartridge neuron differentiation appears unaffected. The 'on/off transients" (representing the activity of post-synaptic lamina cartridge neurons) that are normally seen in wild type are still present.
The overall morphology of lch5 chordotonal organs is disrupted in rhoPΔ38 mutant embryos. In addition, these organs have only 1 cap attachement cell rather than the 2 per organ seen in wild-type, while lch5 ligament attachment cells are often absent or deformed.
Homozygous embryos show loss of VA2 muscle precursor cells (only 2.3% of hemisegments contain VA2 precursor cells).
The number of midline glia cells surviving to stage 16 is decreased to an average of 0.9 +/- 0.1 cells per segment in homozygous embryos.
Mutant embryos exhibit tracheal phenotype.
In stage 12/3 homozygous embryos the commissures are thicker and narrower than wild type and by stage 14 they remain incompletely separated. In stage 12/5 embryos the wild type number of midline glia are present but appear tightly clustered and displayed dorsally. Reduction in cell number from stage 13 until 14. Reduction in the VUM cell number at stage 11, during stage 13 half the wild type number of neurons migrate ventrally, these are still present at stage 14. All MP1 neurons are present at stage 13 but are disconnected from each other, by stage 14 this separation has grown. In stage 14 embryos there is a reduced number of en+ neurons present at the midline.