Expression of ACCGD3482 under the control of Scer\GAL4Desat1.PB leads to significantly increased lipid droplets in larval oenocytes when larvae are fed, and results in significantly decreased lipid droplets when larvae are starved, but does not change oenocyte size in starved conditions, as compared to controls. An increased proportion of larvae expressing ACCGD3482 under the control of Scer\GAL4Desat1.PB display tracheal flooding, as compared to controls.
Flies expressing ACCGD3482 under the control of Scer\GAL4insc-Mz1407 are extremely sensitive to dessication, with significantly decreased survival time during dessication stress, as compared to controls; this phenotype is not seen when ACCGD3482 is expressed under the control of both Scer\GAL4insc-Mz1407 and Scer\GAL80svp.3kb. Oenocytes of flies expressing ACCGD3482 under the control of Scer\GAL4insc-Mz1407 show a dramatic accumulation of lipid droplets as compared to controls.
Expression of ACCGD3482 under the control of Scer\GAL4sal.BO (in combination with a Dicer-2 transgene to enhance RNAi efficiency) results in lethality at the L2/L3 transition, accompanied by tracheal defects.
0-4 hour prepupae expressing ACCGD3482 under the control of Scer\GAL4Cg.PA are not delayed in development and maintain a normal body weight. Total triglyceride concentration is dramatically reduced and glycogen content is dramatically increased compared to wild type, while protein concentration is unchanged and glucose and trehalose levels are not significantly affected. There is no significant decrease in non-esterified fatty acids compared to controls.
Expression of ACCGD3482 under the control of Scer\GAL4sal.BO results in 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.
Co-expression of Scer\GAL80svp.3kb completely suppresses the lethality caused by expression of ACCGD3482 under the control of Scer\GAL4sal.BO.
The tracheal network of animals expressing ACCGD3482 under the control of Scer\GAL4sal.BO 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.
Larvae expressing ACCGD3482 under the control of either Scer\GAL4sal.BO or Scer\GAL4desat1.PB and transferred to blue tinted food medium at the L2 or early L3 stage show blue staining of the spiracles that sometimes extends into the main tracheal trunks, indicating a water-tightness defect in the spiracles.
Expression under the control of Scer\GAL41407 results in an increased number and size of GFP-positive aggregates within neuroblast lineage cells in the larval brain compared to controls (these aggregates may indicate cell death or a disturbance of internal cellular structures).
Adults expressing ACCGD3482 under the control of Scer\GAL4elav.PLu (in the presence of Dcr-2Scer\UAS.cDa to increase the efficiency of RNAi) do not show a significant defect in avoidance of noxious temperature (46[o]C) compared to control flies.