Homozygous germline clones have not been obtained in females.

BrdU incorporation is seen in homozygous third instar larvae, as occurs in controls.

Homozygous animals are morphologically identical to control animals at early stages of larval life, but at later larval stages the growth rates diverge, with homozygous larvae showing a substantially slower, linear growth rate compared to the exponential growth of heterozygous siblings. Although the mutant larvae show defects in growth rate, they moult and on the basis of anterior spiracle and mouth hook morphology, progress through the third instar stage.

The foraging and eating behaviour of homozygous larvae is indistinguishable from that of heterozygous controls. Gut clearance rates of homozygous larvae are significantly lower than those of heterozygous controls. The mutant larvae show a substantial defect in middle midgut acidification, whereas the posterior midgut is basic (as is seen in wild-type larvae). The middle midgut epithelium of homozygous larvae is highly irregular, most notably with respect to copper cell apical plasma membrane morphology; the apical plasma membrane invaginations of the mutant copper cells are distorted, with enlarged, apical membrane invaginations connecting to the gut lumen. The septate junctions are much narrower than normal and show a substantially decreased apical-basolateral orientation.

Mutant larvae show normal levels of uptake of the nutrients glucose and leucine, but uptake of lysine and alanyl-alanine dipeptide is markedly reduced in the mutant gut compared to controls. Mutant larvae show significantly reduced levels of both essential and non-essential amino acids (with the exception of the urea cycle metabolites ornithine and citrulline).

Fat body tissue from homozygous larvae has reduced cellularity and is nearly transparent. The mutant fat body tissue contains 20- to 25-fold less triglyceride per unit phospholipid than in paired heterozygous controls. The cytoplasm of fat body cells of homozygous third instar larvae contains single, very large, prominent lipid vesicles and the nuclei are small and irregular.

Homozygous oenocytes are Oil Red positive (indicating lipid accumulation) in both the fed and starved states, whereas heterozygous oenocytes only show lipid accumulation after starvation.