Homozygotes die at late embryogenesis; they fail to hatch but do not show any obvious morphological defects.

Homozygous clones in the third larval instar fat body have a reduced amount of lipid droplets compared to controls. Homozygous oenocyte clones in late second instar larvae show a dramatic increase in lipid droplets compared to controls.

ACC^B131 animals expressing ACC^Scer\UAS.cPa under the control of Scer\GAL4^da.G32 in the presence of Scer\GAL80^svp.3kb show lethality at the L2/L3 larval transition. The larvae grow normally until the end of the second instar, but are unable to grow further. They survive a few more days, but eventually contract in size before dying between 4 to 5 days after egg deposition. The larvae show abnormal feeding behaviour at the late second instar stage, with more than 50% of the larvae straying away food 1 hour after being placed in a small piece of food in the middle of an agar plate. Oenocytes are visible in late second instar larvae, but they accumulate high amounts of lipid droplets compared to controls.

The tracheal network of ACC^B131 animals expressing ACC^Scer\UAS.cPa under the control of Scer\GAL4^da.G32 in the presence of Scer\GAL80^svp.3kb appears normally filled with air at the first larval instar stage. However, at the L2/L3 transition the larvae found outside of the food show a severe defect in air-filling of their tracheal trunks. The tubes are still distinguishable, suggesting that they are present but filled with an aqueous solution. The air-filling failure is seen in the spiracles and main trunks, but only occasionally extends into lateral branches and the tracheoles.

Acc^B131/ACC[+] is a suppressor of adult heart phenotype of eas²