Imprecise excision of the progenitor insertion, resulting in a deletion that removes the entire first exon (including the ATG initiation codon) of Ppcs.
adult brain (with Ppcs1)
adult fat body (with Ppcs1)
egg chamber (with Ppcs1)
larval brain (with Ppcs1)
7 day old 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/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.
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/Ppcs33 adults compared to controls. The level of phospholipids is also reduced compared to controls.
The pericerebral fat body is almost absent in 14 day old Ppcs1/Ppcs33 adults.
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/Ppcs33 third larval instar brains compared to controls.
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/Ppcs33 animals compared to wild-type flies.
