Homozygous female germline clones result in a fully penetrant dumpless phenotype, with severe defects in oocyte integrity. The oocytes appear normal until stage 9. During stage 10, the anterior region of the oocyte begins to detach from nurse cells and follicle cells. In severely affected egg chambers, the oocyte detaches from the nurse cells completely and the cytoplasm of the nurse cells leaks into the space between the nurse cells and the oocyte. In more mildly affected egg chambers, the oocyte is connected to the nurse cells and intercellular cytoplasm transport occurs to some extent, however, the oocyte fails to grow to the normal size.

The formation of endoplasmic reticulum (ER) clusters is severely impaired in oocytes of homozygous female germline clones; only 17% of stage 9 and 10 mutant oocytes have ER clusters and instead the ER remains dispersed in the cytoplasm in most mutant oocytes. The diameter of the ER lumen does not expand in the mutant oocytes, in contrast to wild-type oocytes. The distribution of the Golgi is unaffected in mutant oocytes.

Yolk granules are reduced in size and abundance in mutant oocytes of homozygous female germline clones, with the overall area occupied by yolk granules being reduced by approximately 70%. The number of coated pits and vesicles is reduced by approximately 60% in these oocytes.

The surface area of the oocyte is reduced compared to wild type in homozygous germline clones. The number of microvilli ranges from a slight reduction compared to wild type to almost complete absence of microvilli.

Homozygous somatic clones result in bristles that are thinner and shorter than wild type. This defect is seen in several bristle types, including wing anterior margin bristles, microchaetae and macrochaetae. The ridged structure of the mutant bristles is abnormal; wild-type bristles contain several parallel ridges with deep valleys between them, but the mutant bristles have a weak ridge structure with shallow valleys.