Homozygous Ts(1Lt;YSt)B118+Ts(1Rt;YLt)T9 mutants exhibit virtually complete loss of commissural fascicles of C4da neurons.

Ts(1Lt;YSt)B118+Ts(1Rt;YLt)T9 embryos show defects in the commissures of the central nervous system; 4% of anterior commissures are thin, 19% of posterior commissures are absent and 20% of posterior commissures are thin. 14% of segments fail to separate the anterior and posterior commissures correctly.

dMP2 axons make pathfinding errors in Ts(1Lt;YSt)B118+Ts(1Rt;YLt)T9 mutant embryos, often extending laterally, turning anteriorly or stalling.

Retinal projections of axons are normal.

Embryos display defects in commissure formation, fewer axons cross the midline than normal. They also exhibit frequent errors in the dorsal projections of the ISN and of the ventral projections of the ISNb. Projections of the SN are unaffected. Scer\GAL4^F63-mediated expression of NetA^UAS.cHa or NetB^UAS.cHa rescues the embryonic phenotype. The RP3 axon extends dorsally past and just adjacent to muscles 7 and 6 and then reached back to innervate them. RP3 neuron may extend into its normal muscle domain but fail to innervate muscles 7 and 6. The ISNb fails to innervate muscles 7 and 6. Reducing levels of Sema2a (Sema2a⁰³⁴⁷⁴) restores normal RP3 innervation. Increased level of Sema2a muscle expression, Sema2a^hs.Tl enhances the RP3 phenotype.