Pak6/+ flies do not exhibit a significantly increased pacing-induced heart failure rate or arrhythmia, do not have significantly different diastolic or systolic intervals, nor any significant disruption in cellular architecture of cardiomyocytes as compared to controls.
In Pak4/Pak6 mutants, the antennal lobes are smaller than those of wild type and the boundaries surrounding individual glomeruli are frequently missing.
Pak6/Pak10 mutant animals have abnormally thick axon bundles in the medulla neuropil in the developing eye and axons terminate in poorly differentiated growth cones.
In Pak11/Pak6 adults the antennal lobes are small and mis-shapen compared to wild-type, and have amorphous neuropil. Antennal glomeruli DM2 and DM3 are severely mis-shapen or split into smaller structures that are scattered randomly around the antennal lobe. The integrity and position of VA11m is unaffected, but it is enlarged and extends into the domains of surrounding glomeruli, in most cases completely engulfing the adjacent VA1d. Projection neurons and glial cells differentiate normally in antennal lobes of the mutants, but dendritic arborization of the projection neurons is more diffuse than in wild-type, and the number of glial processes is somewhat reduced. The development of neurons within the antennae appears normal. In Pak6/Pak4 homozygous pupae 30 hours after puparium formation (hAPF) the pattern of olfactory neurons projections from the antennae is normal. However, once in the antennal lobe, the axonal trajectories are clearly abnormal: instead of forming characteristic tracks, the fibers interweave to form a dense mat.
Motor axons in a Pak6/Pak11 mutant background exhibit guidance defects: segmental nerve (SN)b/d and SNa motor axons often (21 and 22%, respectively) overextend and bypass their target muscles.
The subsynaptic reticulum at the NMJ between muscles 6 and 7 is reduced in size in Pak11/Pak6 third instar larvae compared to wild type.
In Pak6/Pak11 embryos, either the entire Bolwig's Nerve, or a subset of its axons project to ectopic positions. These defects have over a 90% penetrance. About 5% of heterozygotes exhibit some Bolwig's nerve targeting defects.
Adult escapers are uncoordinated and have crumpled wings but are otherwise wild type in appearance. R cell axons extend into the brain normally in Pak6/Pak11 flies. However these fibres do not spread evenly within the lamina and medulla. As a result some regions are hyperinnervated while others lack innervation. In the medulla neuropil, R cell axons fail to find their proper targets but instead terminate as abnormally thick, blunt ended fascicles. A small fraction of the R2-R5 neurons project through the lamina and into the medulla, indicating a modest disruption in ganglion target specificity. Some R1 to R6 axons fail to stop in the lamina, resulting in gaps in the lamina plexus. In addition, R cell axons form abnormally thick bundles between the lamina and medulla. Pak6/Pak11 mutant ommatidia are largely indistinguishable from wild-type, of 898 ommatidia counted in four Pak mutant eyes, only nine ommatidia lacked a single R cell. R cell morphology is normal, as is lamina neuron and glial cell differentiation.