LanA¹⁶⁰/LanA²¹⁶ third instar larvae show an elongated VNC, but no defects in VNC length are observed in either heterozygous control.

The neuromuscular junction is normal in LanA^9-32/LanA²¹⁶ third instar larvae.

The ocellar nerve frequently does not form in LanA mutants. Projections of the ocellar pioneer axons are aberrant. They may fail to grow as far as in wild type, or may extend away from the brain. Sometimes the characteristic pair of ocellar pioneer axon bundles do not form. Instead multiple fascicles form, some of which enter the brain at abnormal positions. Normal or increased levels of ECM surround many structures, including the wing disc and optic stalk. However the ECM in the eye-antenna disc region is reduced. Ocellar pathfinding defects are common. In the extreme case the axons do not leave the epidermis, but extend a short distance within the epidermis. Large bundles of ocellar pioneer axons may abnormally join the fascicles of the ocellar and orbital bristles. These axons eventually stall before reaching the brain. Adult ocellar photoreceptors are born on schedule. Around 50% of LanA mutants show major axon pathfinding defects in the photoreceptor axons of the compound eye. These defects can be detected as early as the 3rd larval instar. The optic stalk is often broad in shape and the axons have a loose and disorganized appearance. The optic nerve is usually split into two or more bundles. Retinal axons form whirls within the retina. Growth cones within the retina extend in abnormal directions and fail to enter the optic stalk. Glial cells are abnormally distributed in the eye.

Adult escapers are lethargic and unable to jump or fly, and tend to die within one or two days after eclosion. They variably show defects in morphology of their eyes, legs (short and bulbous segments and fused or deleted metatarsus and tarsi), wings (venation defects and blistering), antennae, ocelli, post-vertical and ocellar bristles. The eye phenotype reflects alterations in array of hexagonal facets, reduction in numbers of facets, disruption in normal array of lenses, misplaced and extra bristles, fusion of ommatidia, reduction in number of photoreceptors and alteration in number of cone cells.

LanA[+]/LanA²¹⁶ is an enhancer of visible | dominant phenotype of sog^EP7

LanA[+]/LanA²¹⁶ is an enhancer of visible | dominant phenotype of sog^EP11

LanA[+]/LanA²¹⁶ is an enhancer of wing vein phenotype of sog^EP7

LanA[+]/LanA²¹⁶ is an enhancer of wing vein phenotype of sog^EP11