Cultured primary neurons derived from enaGC1 and enaGC1/ena23 embryos show a significant reduction in the number of filopodia compared to control neurons. Mean filopodium length is reduced compared to wild type in these neurons.
The ISNb motor axon shows a bypass phenotype (the ISNb axons fail to enter the ventral longitudinal muscle field and instead bypass along the ISN root) in 99% of hemisegments in enaGC1/enaGC5 embryos.
ena23/enaGC1 and ena210/enaGC1 embryos have reduced longitudinal axons in the central nervous system.
Embryos that are both maternally and zygotically mutant for ena (ena23/enaGC1 embryos derived from females with homozygous ena23 germlines) proceed through gastrulation normally and have normal epithelial integrity. Segmental grooves are deeper than normal in these embryos and persist long after they should have regressed. The leading edge during dorsal closure is often uneven. Most of the embryos fail in head involution. Cells that should lead head involution appear to constrict far more than in wild type, nearly severing the head from the thorax.
Mature embryos that are both maternally and zygotically mutant for ena (ena23/enaGC1 embryos derived from females with homozygous ena23 germlines) show defects in the cuticle; 10% have a dorsal pucker, 37% have a hole in the head, 15% have both a dorsal pucker and a hole in the head and 28% have a large ventral hole.
Mature embryos that are both maternally and zygotically mutant for ena (ena210/enaGC1 embryos derived from females with homozygous ena210 germlines) show defects in the cuticle; 15% have a dorsal pucker, 36% have a hole in the head, 14% have both a dorsal pucker and a hole in the head and 7% have a large ventral hole.
75% of zygotic enaGC5/enaGC1 mutant embryos have a wild-type cuticle, while 21% show puckering along the dorsal midline.
Third larval instar single cell homozygous ddaE and vpda neuron clones show a significant decrease in the number of dendritic ends compared to control clones.
enaGC1/enaGC5 mutants exhibit approximately 2 defects in longitudinal axon guidance per animal. An average of 18% of segments show defects. No embryos exhibit defects in pCC/MP1.
enaGC5/enaGC1 embryos show modest levels of midline crossing errors by axons in the central nervous system.
Most enaGC1/ena210 embryos only have mild defects in head involution.
In ena210/enaGC1 mutant embryos, axons in the central nervous system appear to be less tightly fasciculated and commissural bundles sometimes appear abnormal and wander between commissures. Also there are occasional errors in midline guidance, and axon pathways that do not normally cross the midline sometimes do.
Heterozygotes with enaGC8 have diffuse and loosely bundled longitudinal and commissural axon tracts. Some homozygous embryos exhibit thinning of longitudinal connectives, increased number of axons exciting the CNS from the longitudinal axons or failure of commissural axons to separate into anterior and posterior axon bundles. The overall organisation of the PNS is disrupted, spacing and organisation of the neurons is irregular and some clusters of neurons are mislocalised.