Although the structure of the nervous system is disrupted in mutant embryos and the dendritic arbors are abnormal, they continue to form in their characteristic locations and the fundamental distinction between ISN and SN motor dendritic fields is maintained.

Axonal elongations of the MP1/dMP2 and vMP2 neurons show no obvious abnormality in stage 13 gcm^P/gcm¹ embryos even though most of the misdifferentiated glial cells do not contact these longitudinal pioneer axons. Fasciculation of the MP1/dMP2 and vMP2 axons occurs normally in the absence of glial cells, although elongation is delayed and the fascicle looks thinner in some hemisegments. The dMP2 neurons send out axons in an abnormal orientation in some hemisegments of gcm¹ embryos, occasionally joining with a motor pathway. The pCC pathway is broken or becomes thinner at stage 15. EG glial cells and peripheral glia are missing in stage 16 mutant embryos. The intersegmental and segmental nerves are separated and do not meet at the exit junction in mutant embryos (in contrast to wild type). The segmental nerve exits the CNS at a more ventral position than normal. Axon bundle formation is also affected in the peripheral nervous system. The ISNb motor axon apparently innervates target muscles, however the position of the muscles is sometimes abnormal.

Homozygous embryos exhibit severe axonal defects, longitudinal tracts have fewer axons than normal and the transverse commissures are sometimes fuzzy. There are few glial cells as they are transformed into neurons of the PNS. CNS neuromere remains elongated at the end of embryonic development, a condensation defect. Pioneer neurons can find their correct pathway without the help of glial cells.