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
75% of zygotic enaGC5
mutant embryos have a wild-type cuticle, while 21% show puckering along the dorsal midline.
animals exhibit a weak ISNb bypass phenotype, seen in about 7% of hemisegments.
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.
embryos show modest levels of midline crossing errors by axons in the central nervous system.
86% of ISNb axons show a bypass phenotype in enaGC1
embryos. This phenotype is partially suppressed by enaScer\UAS.cCa
expressed under the control of Scer\GAL4neu
. 29% of ISNb axons show a bypass phenotype in enaGC5
embryos. A small number of RP neurons follow an aberrant path within the central nervous system.
Lethal in combination with enaGC1
Heterozygotes with enaGC8
have diffuse and loosely bundled longitudinal and commissural axon tracts and some also exhibit axon misguiding. 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.