Pten5/Ptendj189 flies exhibit a highly penetrant, but mild, disorganised eye phenotype at the posterior edge in the midline.
Pten5/Ptendj189 mutant males show significantly increase susceptibility to oxidative stress by paraquat, inhibition of mitochondrial complex by rotenone, osmotic stress by NaCl, and water-only starvation compared with wild-type controls.
The size of the wings is increased in Ptendj189 heterozygotes compared with wild-type.
Expression of PtendsRNA.Exel.Scer\UAS under the control of Scer\GAL4C57 in the muscles in a Ptendj189/+ background results in a significant decrease in the number of synaptic boutons at the larval neuromuscular junction.
Larvae expressing PtendsRNA.Exel.Scer\UAS under the control of Scer\GAL4C57 in the muscles in a Ptendj189/+ background show no increase in evoked excitatory junctional potential (EJP) amplitude compared to controls, although the amplitude and frequency of miniature EJPs is increased in these animals compared to wild type.
Ptendj189 mutants show no defects in opsin regulation.
Homozygous embryos derived from homozygous female germline clones show severe abnormalities even in freshly laid eggs; the eggs are generally smaller and more roundish than wild type and many do not show any development. In those embryos that do initiate development, formation of pole cells is rarely seen, and where they do form, they are typically only 2 or 3 in number (compared to an average of 35 in wild type). In those homozygous embryos derived from homozygous female germline clones that do show development, axial expansion (the spreading out of nuclei along the long axis of the embryo in cycles 4-7) does not occur, resulting in a spherical rather than ellipsoid arrangement of nuclei prior to cortical migration and an abnormally low nuclear density in the posterior region of the embryo at the syncytial blastoderm stage. The synchrony of the cell cycle during cleavage divisions is lost (the pattern of mitoses is not completely randomised, but occurs in waves that always start at the posterior of the embryo). This results in blastoderm nuclei with different morphology and different condensation states of chromatin in distinct regions of the embryo at the beginning of cellularisation. The cellularisation front advances much more rapidly in the anterior of the mutant embryo compared to the posterior, and the delay in cellularisation at the posterior pole is often accompanied by severe defects in gastrulation, which often results in the rapid degeneration of the mutant embryo shortly after the onset of gastrulation. However, some mutant embryos recover well from the early developmental defects and complete embryogenesis without any gross morphological abnormalities. Survival beyond gastrulation is independent of whether the embryos receive a wild-type paternal copy of Pten. Stage 10 egg chambers in females containing homozygous germline clones have a very disorganised actin cytoskeleton which fills the nurse cell cytoplasm instead of localising to the cell borders. Fusion of nurse cells is often seen, as are mispositioned nurse cell nuclei that appear to have moved into the oocyte.
Homozygous mutant clones of Ptendj189 in the eye produce ommatidia that are larger than wild-type and often bulge out of the eye. Eye bristles are also larger. Mutant photoreceptors are increased in area by about 140% compared to wild-type. Quantitative examination reveals that homozygous Ptendj189 clones contain on average 3.2 times as many cells as their twin spot controls. The intervening non neuronal cells in these clones are probably increased in size. In clones that included the whole eye, the number of ommatidia increases from about 750 (in wild-type) to about 1075, the area of the eye increases by at least 55%. Clones in the wing margin leads to a smaller number of larger bristles along the margin. In embryos produced from germ-line clones of homozygous Ptendj189 no increase in apoptosis is seen.