In poe¹ mutant spermatids, the "individualisation complex" (precursor of the cystic bulge) is significantly reduced, or undetectable, and no cystic bulges form. However, caspases activity is clearly detectable in elongated spermatids that lack an individualisation complex.

Mutants exhibit a normal axon and peripheral glial layer, but a thickened perineurial glial layer.

Behavioural defects including sluggishness, uncoordination and defects in flight. When pushed onto the dorsal surface by mechanical agitation flies require an average of 46 seconds to right themselves, 20-fold more time than required for wild type. Male sterility is not a result of defective mating behaviour but rather of a downstream effect, such as sperm function. Mutant larvae exhibit a two fold increase in excitatory junctional potential (ejp) over wild type at an external calcium concentration of 0.15mM and an increased frequency of miniature excitatory junction potentials (mejps). Quinidine application at an external calcium concentration of 0.4mM or 1.0mM led to muscle depolarisations that were extremely prolonged in duration compared to wild type. These effects on synaptic transmission are due to prolonged transmitter release at the neuromuscular junction.

poe¹ has CNS surface glial cell phenotype, enhanceable by Nf1^P2

poe¹ has CNS surface glial cell phenotype, enhanceable by ine¹