Pten5/Pten1 flies exhibit a highly penetrant, but mild, disorganised eye phenotype at the posterior edge in the midline.
Transheterozygous mutant Pten5/Pten1 males have significantly (~20%) greater body mass than wild-type.
A small proportion of newly eclosed Pten5/Pten1 flies display outstretched and paralysed wing phenotype. The flies are unable to fly. The proportion of flightless mutant increases as flies age.
The integrity of the follicle cell epithelium is not compromised in egg chambers containing homozygous follicle cell clones.
Somatic clones of homozygous Pten1 mutant future-intervein cells display disrupted hexagonal packaging. In the mutant tissue, only 50% of the cells are six-sided. Furthermore, the tissue exhibits cell patterns with distinctive local cobblestone patterns and some rosette patterns. The cobblestone pattern refers to hexagons with two sides much shorten than the others.
Pten1 mutant ddaC neuron clones exhibit dendrite pruning defects at 16 hours after puparium formation.
Pten1 mutant somatic clones generated in the eye display highly disorganised ommatidia with compromised apical membranes. There is a failure of rhabdomere morphogenesis, and most photoreceptors display abnormally elongated, deformed, or split rhabdomeres. These defects are evident from mid-pupal development onwards. There is no evidence of photoreceptor degeneration in retinas from a series of aged adult flies.
Nurse cells in 90% of Akt11 mutant clones show cell-autonomous formation of large aggregated droplets and a corresponding reduction in small perinuclear droplets compared to wild-type nurse cells.
Mutant clones in the adult eye produce large cells and misrotated ommatidia. Cells in mutant clones in the eye disc show precocious differentiation several rows ahead of wild-type cells. In addition, ommatidia within clones in the eye disc initiate rotation before wild-type ommatidia.
Mosaic animals in which the eye is largely homozygous for Pten1 (generated using the "eyFLP" system) have larger eyes than normal. The eyes contain about 12% more ommatidia than wild-type eyes and individual ommatidia are 78% larger in surface area.
Hemizygotes die as late embryos or early first instar larvae. Homozygous mutant clones in the eye bulge out from the eye surface. Ommatidia sometimes fuse interommatidial bristles are abnormal, particularly (but not exclusively) in the dorsal half of the eye. Mutant clones typically contain at least twice as many ommatidia as their wild type twin spots. The largest clones can form a hyperplastic tumor-like overgrowth, though this phenotype is less severe than for tumor suppressor mutations. Within each ommatidium cell type specification seems normal. Cell bodies of mutant photoreceptors are enlarged compared to wild type neighbors, and the rhabdomeres are misshapen. The cell size and rhabdomeric phenotypes are cell autonomous. Homozygous mutant clones in the wing reveal an increase in cell size. Wing hairs are occasionally duplicated and crossvein formation is abnormal. Occasional extra wing vein material develops. Longitudinal veins are rarely affected.