Apoptosis is seen in the wing pouch area of homozygous third larval instar wing imaginal discs (no cell death is seen in wild-type wing discs at the same stage).
mutant third instar larvae have significantly smaller wings discs compared to controls and are developmentally delayed.
homozygous females and hemizygous males all die during pupation before any adult structures are formed although their growth rate and size during larval stages is unaffected. Onset of pupariation however is significantly delayed by around 32 hours compared to wild-type, the larvae continue to feed during this period and are thus significantly heavier just before pupariation than controls.
transheterozygote adults cannot emerge from their pupal cases and remains stuck. The same phenotype is seen when pcm5
is combined with Df(1)ED7452
deficiency, suggesting that pcm14
is genetically a null allele.
homozygote third instar larvae have significantly smaller wing, metathoracic leg, haltere as well as eye imaginal discs compared to wild-type controls. The wing discs are also delayed both in growth and differentiation (assessed by wg
pattern) and even though the entry into pupal stage is delayed in pcm14
homozygotes, their wing discs just before the onset of pupariation are still significantly smaller compared to controls.
third instar larval wing discs display significantly increased level of apoptosis (assessed by Caspase-3 staining). However, both the mitotic and the S-phase index (calculated as number of cells per area) are also increased compared to wild-type, suggesting the wing disc cells are dividing more to counteract the cell loss due to apoptosis.
Somatic clones of pcm14
cells in the third instar larval wing discs are much smaller compared to their wild-type twin spot counterparts.