P5CDh1^f04633/P5CDh1^f04633 mutants show significantly reduced hatching rate, most of them die during larval stages and none eclose as adults. They also show severe growth defects as the P5CDh1^f04633 homozygote larvae are significantly smaller than wild-type controls and on the ultrastructural level display mitochondrial defects (swollen mitochondria with depleted matrices) in the polyploid cells of larval midgut.

P5CDh1^f04633/+ animals develop normally with no apparent growth defects.

P5CDh1^f04633 homozygotes show several growth defects. About 50% die during embryonic stages. First instar larvae emerge from the remaining eggs but only one third of these survive to the pupal stage. Larvae that survive beyond the second instar experience a prolonged third instar stage, while those that survive to the pupal stage are stunted in their growth. No homozygous pupae eclose as an adult.

Homozygous P5CDh1^f04633 larvae show a two-fold increase in proline levels compared to wild type, whereas Glu/Gln, Asp/Asn and Tyr levels are all reduced compared to wild type.

Mitochondria from the midgut of P5CDh1^f04633 homozygotes appear swollen. Cristae are clearly evident but their central matrices appear empty. The average transverse diameter of mutant mitochondria is 54% greater than that of wild type mitochondria.