No tracheal defects are observed in homozygous mutants.

Homozygotes grow more slowly than controls and die at the L1 or L2 stage. These larvae are consistently much smaller than controls, exhibit little or no coordinated locomotion, fail to show effective feeding, and exhibit developmental delay. In extreme cases, homozygotes are unable to crawl out of their eggshells and die within a few hours of hatching. Heterozygotes show no difference from wild type.

Stage 15 homozygous embryos show an essentially wild-type pattern of musculature.

Stage 15 homozygous embryos show malformation of the ventral nerve cord (VNC), with a lack of some commissures, breaks in the longitudinal connectives, and the presence of underdeveloped commissures, resulting overall in a widening of the distance between longitudinal connectives of the VNC. They also exhibit a marked loss and hypoplasia of neurons in the peripheral nervous system (PNS), evidence of neuronal degeneration, disorganization of the neuronal pattern in the central and peripheral nervous systems, and severely malformed developing eye discs. Anti-futsch staining shows that homozygous mutant embryos exhibit severe disruption, disorganization and loss of both PNS and VNC neuron and/or neurite subsets.

Anti-eve staining shows that homozygous mutant embryos exhibit a less well organized and defined central nervous system, although the anal plate staining in well organized similar to wild type.

Anti-Fas2 staining shows that homozygous mutant embryos exhibit severe abnormalities in the ventral nerve cord, extensive hypoplasia of developing eye discs and, in the brain, axon mislocalization and a reduction in the number of motor neurons and abnormalities in their organization.

Anti-ct staining shows that homozygous mutant embryos exhibit massive abnormalities in the structure of developing Malpighian tubules and in the anterior and posterior spiracles, together with a severe loss of neurons in the CNS.

A dramatic disorganization of glia is observed in stage 15 homozygous embryos.

In squashed testis preparations, spermatocytes as well as elongated spermatid bundles are present n young pex1^s4868 mutants. At the onion stage, most round spermatids are abnormal. Spermatids usually have four nuclei and one large mitochondrial derivative, indicative of a cytokinesis defect. This phenotype progressively worsened with age. In older mutant animals, 'cotton ball'-like spheres are also present.