Mutant embryos develop ectopic sclerites, which often look like the cuticular scar tissue that often surrounds the healed wound generated by a sterile needle in late-stage wild-type embryos.
Mutant stage 17 embryos have failures in epidermal integrity; dye injected into the perivitelline space penetrates the body cavity in the mutant embryos.
Generation of spenpoc361 mitotic clones in the wing imaginal disc, using the FLP/FRT technique, causes a wing vein phenotype in the adult. This includes loss of vein material, which is mostly in the distal part of the wing, ectopic formation of material around the veins, thickening of existing veins and slight mis-localization of both longitudinal and cross-veins. Wing hair polarity is also disrupted and bristles are misplaced at the wing margin. Generation of spenpoc361 mitotic clones in the anterior compartment of the wing disc, using the FLP/FRT technique, affects both the micro and macrochaetae on the notum of adults. Macrochaetae are lost in some parts of the notum, gained in others and mislocalized. Duplicated trichogens and thormogens are not observed, indicating that cell fate specification is not affected. In both spenpoc361 maternal and zygotic embryos, the neurons of the peripheral nervous system show an abnormal distribution and morphology, and can be either fewer or greater in number than in wild type.
Mutant embryos derived from females containing homozygous spenpoc361 germline clones crossed to spen3/+ males (lacking both maternal and zygotic spen function) show alterations in the number of many peripheral and central nervous system cell types, and the development of other organs is affected. The number of lateral chordotonal organs in each abdominal hemisegment varies from 0 to 6, and is typically 4 (wild-type number is 5). Clusters containing the normal number are often disorganised. Midline development is defective. Commissures are missing or poorly separated in stage 15 embryos. All of the longitudinal axons are disrupted in stage 16 embryos and axons inappropriately cross the midline. The development of all motor axons pathways is defective; motor axons exit the central nervous system, pick the correct pathways, but fail to innervate their muscle targets. Muscle fibres are missing or disorganised.
Hemizygotes show loss of anterior H piece and ectopic sclerites develop in the middle of T2 and T3. These ectopic sclerites do not form in the fields of the denticle belts. When the maternal contribution is reduced the phenotype is more marked, with the posterior mouth hooks, median tooth, hypostomal, ectostomal, and epistomal sclerites, dorsal bridge and lateralgraten all either missing or disrupted. The trunk region of the embryos appears to be largely unaffected. Denticle belts and filzkorper show slightly reduced pigmentation.