When msnDN.Scer\UAS is expressed in the developing eye of wild-type animals R-cell precursors migrate as normal. When expressed in msn03349/+ animals a highly penetrant nuclear migration phenotype is seen.
Almost no msn03349 homozygous flies eclose and a large proportion of those that do have thorax closure defects.
Many R1-R6 growth cones fail to stop at the lamina layer in msn03349/msn102 larvae. Most msn03349 animals die at the late pupal stage. msn03349 third instar larvae have a mild defect in photoreceptor cell axonal projections. The lamina plexus is uneven. Only 5% of msn03349 animals expressing msnD160N.Scer\UAS under the control of Scer\GAL4elav.PLu survive to the pupal stage.
Lethality acts during the larval and pupal stages.
The photoreceptor cell growth cones are able to extend into the developing optic lobe in homozygous third instar larvae, but their innervation patterns within the lamina and medulla are altered compared to wild type. Gaps are seen in the lamina R1-R6 termination site and abnormal, large bundles of axons are seen in the medulla. Growth cone morphology is altered, although the photoreceptor cell growth cones are able to expand upon reaching the target. The severity of the phenotype is variable.
Germline clones produce eggs with patterning defects: embryos are twisted with variable cuticle differentiation.
Homozygotes late to eclose.