A low but significant frequency of axon defects are found in embryonic motor neurons, consistent with a defect in axon targeting. Hemizygotes show guidance defects in 1.4%, 8.1% and 6.9% in ISN, SNa and ISNb neurons respectively. No defects are seen in neuroblast polarity, mitotic spindle orientation, cell fate determination, or epidermal integrity are seen. In maternal and zygotic nulls, embryos display a range of abnormalities in their VNC axons: thinning of longitudinals, abnormal midline crossing and wandering trajectories, axon tangles, axon breaks, collapse or thinning of the anterior and posterior commissures and defasciculation. 25.3%, 55.0% and 60.1% of ISN, SNa and ISNb neurons show guidance defects respectively. The ISN display defects such as stalling/splaying defasciculation, and failure to innervate targets. The SNa exhibit missing or truncated dorsal lateral branching, ar abnormal defasciculation. ISNb axons often dislay abnormalities such as failure to innervate the clefts between muscles 6/7 and 12/13, premature arrest, failure to defasciculate from the ISN and bypass of targets.
pod1Δ96 is partially rescued by pod1UAS.GFP,Tag:MYC/Scer\GAL4elav.PLu