TorΔP/TorΔP fat body clones in a Minute background, induced during embryogenesis and analyzed at early third instar larval stage, are small and bear smaller cells than controls.
TorΔP homozygous somatic clones in third instar larval eye discs exhibit a delay in G1/S transition during the second mitotic wave, as mutant cells enter S phase in a more posterior region than control cells.
Electroretinograms (ERGs) recorded from TorΔP/TorΔP full eye clones show significantly reduced amplitudes and off transients compared to controls. TorΔP/TorΔP full eye clones are reduced in size compared to controls. TorΔP/TorΔP mutants exhibit slow growth and developmental delay. TorΔP/TorΔP mutants in egg chamber follicle cells show reduced clone and cell size.
TorΔP larvae show relatively mild dendrite growth defects in the large C4da dendritic arbors.
TorΔP/+ heterozygote adults are significantly lighter compared to wild-type. The females eclose slightly earlier under standard nutrition than wild-type but at the same time as wild-type if nutrition is limited. Adult females have smaller wings as the cells are smaller compared to wild-type but their number is not changed.
TorΔP/+ flies have eyes similar to wild-type.
In TorΔP germline clones, 67% of eight-cell cysts contain pro-oocytes that have prematurely transitioned from the mitotic to the meiotic cycle.
TorΔP MARCM neuroblast clones exhibit developmental axon regrowth defects.
Homozygous dendrite arborization neuron clones show a severe and highly penetrant simplification of the dendritic arbors, with significant reductions in both the number and length of dendritic branches.
In the eye imaginal discs, TorΔP mutant cells proliferate more slowly than their wild-type twin spot control cells.
Cells in homozygous clones in the fat body are 70% smaller than surrounding wild-type cells.
Mosaic TorΔP mutant clones show a nearly complete block of TR-avidin uptake.
BrdU incorporation is normal in somatic clones of TorΔP homozygous cells in the late third instar eye disc.
Loss of Tor activity causes induction of autophagy in normally fed animals. Larvae show reduced size, as do the cells of the fat body. Lethality occurs late in the larval stages.
Clones of TorΔP homozygous wing disc cells show a marked reduction in cell size and an increase in the population of cells in G1 compared to wild-type cells from the same discs.
Homozygotes hatch at normal rates, but grow more slowly than normal and eventually arrest during larval development, reaching only 24% the mass of wild-type controls. The mutants remain viable and active during an extended larval period of about 30 days and eventually die without pupating. Homozygous somatic clones in the adult produces mutant cells markedly reduced in size. Clones in the wing are approximately half the size of controls. When TorΔP clones are compared to wild-type sister clones, in developing imaginal discs, they are similar in size 48 hours after induction, but by 72-96 hours they contain significantly fewer cells. In addition lone twin spots lacking a mutant sister are occasionally observed, indicating that at some frequency TorΔP homozygous cells are eliminated from the disc epithelium. FACS analysis of clones in the developing imaginal discs reveals a decrease in cell size of 30% observed in all phases of the cell cycle. Cell cycle phasing is also considerably different to that of controls, with relatively more cells in G1. and fewer in S and G2 phases. When salivary glands are examined from TorΔP mutant larvae a phenotypes affecting both polytene gland cells and the imaginal ring cells are seen. The endoreplicative cells undergo only four or five rounds of replication before entering quiescence, reaching a ploidy 16 ro 32 C and a size about 10% of wild-type. The imaginal rings of these larvae contain approximately fivefold fewer cells than wild-type. When homozygous mutant clones are examined in the wing imaginal disc, the nucleolar area is approximately half the size seen in wild-type cells. Also the appearance of fat body cells in the larva is changed by an aggregation of lipid vesicles. At 3-4 days after egg deposition (AED), both endoreplicative and mitotic tissues are found to cycle normally in TorΔP homozygotes (as measured by BrDU incorporation). In contrast, by 5-6 days AED all endoreplicative tissues including the gut fat body and salivary glands fail to incorporate BrDU. Whereas neuroblasts continue to cycle. The same is seen at 10d AED.