The germaria of homozygous females show incomplete follicle cell migration and fusion of cysts. Cysts in region 2b of the mutant germarium do not show the characteristic lens-shape, indicative of aberrant cyst encapsulation.

Homozygous ovarioles contain egg chambers with multiple or mispositioned oocytes. The mispositioned oocytes do not have more than the normal amount of 4 ring canals.

Stage 3-6 homozygous egg chambers with mispositioned oocytes have ectopic polar follicle cells.

The mitotic-to-endocycle switch is intact in homozygous egg chambers and no mitotically active follicle cells are seen after stage 6.

Homozygous germaria show aberrant formation of the interfollicular stalk that normally separates neighbouring egg chambers; some egg chambers are not separated by interfollicular stalk cells, while other egg chambers are separated by elongated stalks containing undifferentiated follicle cells.

No defects in follicle cell proliferation are seen (no major gaps in the follicular epithelium are detected), but follicle cells accumulate in a bilayer at the posterior of the oocyte in some homozygous egg chambers.

41.6% of homozygous egg chambers have supernumerary nurse cells, and the ratio of nurse cells to oocytes is not always 15:1 .

Homozygous egg chambers and germaria are apoptotic, with apoptosis being most profound in the follicle cells (some apoptotic nurse cells are also seen).

Dorsal appendage and operculum formation is disrupted in homozygous stage 13 egg chambers.

Nurse cell chromatin morphology is affected in stage 6-8 homozygous egg chambers; 34.2% of egg chambers have normal chromatin, 11.8% have aberrant chromatin and 12.4% have degenerative chromatin.

Homozygous wings have ectopic veins between longitudinal veins L3-L4 and L4-L5. The thorax has ectopic scutellar bristles.

The ovaries of homozygous females are small compared to those of wild-type females 48 hours after eclosion, and the mutant ovaries do not contain mature eggs. At 72 hours after eclosion, only 11% of homozygous ovaries contain vitellogenic egg chambers (compared to 100% of wild-type ovaries at this stage). At 120 hours after eclosion, 80% of homozygous ovaries contain vitellogenic egg chambers, but the two lobes of the ovary are often different in size and show features of degenerating egg chambers.

Homozygous females deposit 0.03 (+/- 0.02) eggs per 24 hours between 144-192 hours after eclosion, compared to 10.00 (+/- 1.4) eggs/24 hours in wild-type females. None of the eggs laid by homozygous females hatch.

Homozygous ovaries at 144 hours after eclosion have a 6-fold increase in ovarioles containing apoptotic egg chambers compared to wild-type ovaries.

Approximately 32% of homozygous ovarioles contain stage 5-7 egg chambers with abnormal amounts of germ-line cells.

Homozygous stage 10-11 egg chambers show a number of defects; 20.9% have nurse cells trapped inside the oocyte, 50.1% have F-actin clumps in the ooplasm, 92.2% have aberrant F-actin in nurse cells, 71.0% have nurse cells plugging the ring canals, 43.7% have oocytes with disorganised subcortical F-actin and 18.8% have oocyte nuclei encapsulated by F-actin fibres.

Migration of the centripetal migrating follicle cells occurs normally in homozygous egg chambers, but nurse cells are observed within the oocyte compartment after these cells have finished their migration. Centripetal migration is finished in the mutant egg chambers before the border cells reach the anterior of the oocyte, indicating that these two cell migration events are not properly synchronised in the mutant egg chambers.

Neutral lipid synthesis is reduced compared to wild type in homozygous nurse cells.

80% of the eggs laid by homozygous females have a dumpless phenotype.

Eggs laid by homozygous females show a wide array of chorion patterning defects; 7.5% have opercula positioned at a different angle in relation to the stalks and have 4 dorsal appendages, 24.7% have abnormal dorsal appendage stalks, 14.5% have fused dorsal appendages, 21.5% lack dorsal appendages and the remaining 22.8% have either 2 dorsal appendages of different lengths, missing paddles or a shift of dorsal appendages posteriorly.

No vitellogenic egg chambers are seen in Ppcs¹/Ppcs³³ females.

Homozygous males show defects in cytokinesis during spermatogenesis; the mutant spermatids contain big Nebenkern structures associated with 2 or 4 nuclei and contain abnormally persistent mitochondrial bridges. Approximately 17% of homozygous males have testes with more than 10% of abnormal spermatids.

Approximately 82% of Ppcs¹/Ppcs³³ males have testes with more than 10% of abnormal spermatids.

Homozygous larvae show normal crawling activity.

Homozygous adults become paralysed after heat exposure (2 hours at 37[o]C) and recover to near normal activity 15 minutes after being placed at 22[o]C.

Follicle cells of stage 3-7 follicles are frequently positive for TUNEL staining in homozygous females.

7 day old Ppcs¹/Ppcs¹ and Ppcs¹/Ppcs³³ flies show a decrease in the fraction of flies able to initiate flight compared to controls. This phenotype is more severe in 14 day old homozygous flies and the aged flies show reduced flight performance compared to the young flies.

Ppcs¹/Ppcs¹ and Ppcs¹/Ppcs³³ 7 day old flies show a reduced ability to climb compared to control flies in a negative geotaxis assay. 14 day old homozygous flies show no difference in performance in the negative geotaxis assay compared to 7 day old homozygous flies.

Homozygous flies have a reduced median lifespan (42 days) compared to control flies (50 days).

Ppcs¹/Ppcs¹ and Ppcs¹/Ppcs³³ flies often have held-out or (less frequently) held-up wings.

The brains of 30 day old Ppcs¹/Ppcs³³ flies contain vacuoles, suggesting neurodegeneration. Degeneration of the photoreceptor cells is visible by loss of retinal structure and vacuoles within the retina.

The level of triglycerides is reduced approximately 25% in 14 day old Ppcs¹/Ppcs¹ and Ppcs¹/Ppcs³³ adults compared to controls. The level of phospholipids in 14 day old Ppcs¹/Ppcs³³ adults is also reduced compared to controls.

The pericerebral fat body is almost absent in 14 day old Ppcs¹/Ppcs³³ adults.

Homozygous adults show increased sensitivity to 5% H[[2]]O[[2]] and 100mM dithiothreitol but not to 20mM paraquat compared to control adults.

Homozygous larvae show reduced survival on medium containing 100mM cysteine compared to control larvae.

Homozygous third larval instar brains do not show mitotic defects.

Ppcs¹/Ppcs³³ third larval instar brains show a high incidence of abnormal mitotic chromosomes compared to controls.

Treatment with 20 Gy irradiation results in an increased incidence of abnormal mitotic chromosomes in Ppcs¹/Ppcs¹ and Ppcs¹/Ppcs³³ third larval instar brains compared to controls.

Ppcs¹/Ppcs¹ and Ppcs¹/Ppcs³³ larval brains show an increased level of apoptosis compared to controls.

The survival rate of adults after exposure of larvae to 20Gy irradiation is reduced in Ppcs¹/Ppcs¹ and Ppcs¹/Ppcs³³ animals compared to wild-type flies.

Ppcs¹ has abnormal locomotor behavior | adult stage phenotype, non-suppressible by Sod1^+t2.4/Cat^tOa/Trxr1^+t10

Ppcs¹ has radiation sensitive phenotype, non-suppressible by Sod1^+t2.4/Cat^tOa/Trxr1^+t10