PpV^X9 germline clones exhibit nurse cell degeneration at stages 9-10 of oogenesis, although follicle cell clones do not show changes in cell number, as compared to control clones.

Eggs derived from PpV^X9 germline clones have apparently normal shape and size but about half of them stop development at the preblastoderm stage, with mitotic defects and mitotic arrest: the nuclei number frequently deviates from the power basis 2; nuclear envelopes lack the LaminDm0 marker, and there are multiple unusually large nuclei. The surviving syncytial embryos frequently undergo an extra nuclear division cycle, despite of unperturbed cell cycle length and decreased nuclei number and density; there is frequent chromosome mis-segregation and chromosome bridges; aborted cytokinesis events, with the resulting nuclei not fully decondensing and undergoing nuclear fall-out in the following interphase; astral microtubules are frequently undetected or less prominent than controls, despite normal spindle assembly/disassembly; there are no defects in centrosome duplication and positioning, centromere number and nuclear envelope dynamics. Part of the surviving embryos fail to extend the germband, although there are no A-P patterning defects. Some embryos survive beyond the blastoderm stage until the end of embryogenesis, form normal cuticle, but fail to hatch.

The progeny of PpV^X9 heterozygous mothers and control fathers exhibit some mortality during the embryonic, larval and Pupal stages, as compared to controls.

PpV^X9 somatic clones in the wing are observed as frequently as control clones.