Young (less than 10 days old) males heterozygous for Psn^I2 do not show any defects in their courtship behavior or locomotor activity compared to wild-type. Their learning index during training with mated unreceptive female is also normal as is their immediate recall memory (assayed by measuring courtship behavior of a male which has just completed a training with a mated unreceptive female toward a receptive virgin female) and 60 min short-term memory (courtship of the trained male is assayed after a 60 min break).

30-day old males heterozygous for Psn^S3 also do not show any defects in the level or quality of naive courtship, locomotor activity, phototaxis or chemotaxis, however they display learning defects (fail to demonstrate the typical decrease in courtship activity when paired with an mated unreceptive female) as well as loss of short-term (60 min) memory is impaired (immediate recall memory is normal though).

Hemizygotes show late prepupal lethality, at the P4(i) prepupa stage.

Mutant larvae secrete a pupal case and complete the last stages of larval development but do not form any adult structures. They collapse into a homogeneous oily mass within the pupal case. The phenotype closely resembles that of Su(H) mutants. Wing margin structures are missing from mutant wing discs. Size of wing pouch is reduced. Clusters of supernumerary SOP cells arise at the position of normal SOP cell emergence. Lateral inhibition in the clusters is impaired. Embryos deficient for maternal and zygotic Psn, derived by fertilization of Psn^S3 germline clone-derived eggs by Psn^B3 sperm, show neural hyperplasia of the embryonic nervous system, and the maternal phenotype is only weakly rescued by wild-type paternal zygotic Psn function.