The viability of ph-p^P1 Trf2^P1 double mutants is strongly decreased. Mortality is seen at the late embryonic stage (approximately 50%) and larval and pupal stages (approximately 30%). Approximately 10% of double hemizygous males and 1% of double homozygous females survive to adulthood. The adults die in 5 to 10 days after eclosion. The double homozygous females are completely sterile and the double hemizygous males have decreased fertility. Approximately 30% of the adults have an extreme transformation of arista to tarsus. The adults have shortened bodies.

Approximately 10% of ph-p^P1 Trf2^P1 double mutant embryos have defects in central nervous system development, and approximately 20% of the mutant embryos have defects in the ventral and lateral clusters of the embryonic peripheral nervous system. Defects in segment organisation are seen in approximately 15% of the embryos.

The karyosome often appears more diffuse than normal in ph-p^P1 Trf2^P1 double mutant oocytes. ph-p^P1 Trf2^P1 double mutant ovaries contain few mature oocytes and have abnormally shaped egg chambers. The ovarioles often contain several follicles that have not separated from the germarium. Many egg chambers contain more than the normal number of 16 nuclei, representing joint cysts packaged inside a monolayer of follicle cells.

ph-p^P1 Trf2^P1 double mutant males have thinner testes than wild-type males. No abnormalities are seen in young primary spermatocytes, but at later stages, many primary spermatocytes show differentiation defects; the chromosome bivalents look more diffuse during metaphase, and aberrant spindles are seen. A significant number of cysts in the mutant testis contain abnormal mature spermatocytes that are probably necrotic.