Homozygotes are viable with normal external adult morphology. While these animals display normal ommatidial development, cortical axon misprojection in the medulla results in neuropil gaps and ectopic axons in the cortical cell body layer, and photoreceptor axon projection defects are observed in the lamina.
Only 12% of EphrinRS5 mutants examined exhibit multiple gaps in the medulla neuropil, while most have no gaps. 24% of mutants show moderate defects and 47% show mild defects in lobula architecture. Large HRP[+] cortical inclusions are rare.
EphrinRS5 has abnormal neuroanatomy | third instar larval stage phenotype, enhanceable by Reph1/Reph[+]
EphrinRS5 has abnormal neuroanatomy | third instar larval stage phenotype, enhanceable by Rephk08617A/Reph[+]
EphrinRS5 has lobula | third instar larval stage phenotype, enhanceable by Reph1/Reph[+]
EphrinRS5 has lobula | third instar larval stage phenotype, enhanceable by Rephk08617A/Reph[+]
EphrinRS5 has medulla anlage | third instar larval stage phenotype, enhanceable by Reph1/Reph[+]
EphrinRS5 has medulla anlage | third instar larval stage phenotype, enhanceable by Rephk08617A/Reph[+]
All optic lobe phenotypic features associated with EphrinRS5 are exacerbated by heterozygosity for Reph1 or Rephk08617A.