Df(2R)Sema2b-C4 homozygous adults exhibit overall central complex morphology and fan-shaped body neuron lamination defects when compared to controls.
Df(2R)Sema2b-C4/Df(2R)Sema2b-C4 larvae (but not Df(2R)Sema2b-C4/+) display increased dendritic non-contacting crossing in the class IV dendritic arborizing (da) neurons, this phenotype is stronger than in Sema2bf02042 mutants.
The requirement for Sema2b to prevent dendritic non-contacting crossing in the class IV da neurons is non-autonomous (Df(2R)Sema2b-C4/Df(2R)Sema2b-C4 neurons in MARCM somatic clones do not display increased dendritic self-crossing).
ISNb axons of homozygous Df(2R)Sema2b-C4 mutant embryos show frequent defasciculation defects at muscle 12, innervation defects at muscles 6/7, and abnormal growth cone morphologies, as compared to controls. SNa axons of homozygous Df(2R)Sema2b-C4 mutant embryos sometimes fail to innervate muscle 24, resulting in a 'stall' phenotype, as compared to controls.
46.3% of hemisegments show disorganisation of the intermediate Fas2-positive longitudinal tract in homozygous embryos. Chordotonal organs fail to elaborate their characteristic morphology within the central nervous system, most often terminating in a position that is lateral to where the intermediate Fas2-positive longitudinal tract normally forms and failing to form a continuous longitudinal branch between segments.
Mutant larvae do reduce their speed significantly in response to vibration, but they show no head turning, in contrast to wild-type larvae.