flightless (with Pten5)
wing & cell | somatic clone
Homozygous clones in the eye disc result in strong overgrowth of the eye.
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.
Pten3/Pten5 has flightless phenotype, suppressible | partially by Akt1[+]/Akt1
Df(2L)flp170B/Pten3 has lethal | late third instar larval stage phenotype, suppressible | partially by Akt1[+]/Akt1
Df(2L)flp170B/Pten3 has lethal | late third instar larval stage phenotype, suppressible | partially by gigUAS.cTa/Scer\GAL4arm.PS/Tsc1UAS.cGa
Df(2L)flp170B/Pten3 has lethal | late third instar larval stage phenotype, suppressible | partially by wdbGS9548/Scer\GAL4arm.PS
Pten3 has hyperplasia | somatic clone phenotype, suppressible by rictorΔ2
Pten3 has eye | somatic clone phenotype, suppressible by rictorΔ2
77% of Pten3/Df(2L)flp170B animals survive to adulthood in the presence of Akt11/+.
Expression of Tsc1Scer\UAS.cGa and gigScer\UAS.cGa under the control of Scer\GAL4arm.PS rescues lethality in 40% of Pten3/Df(2L)flp170B animals.
Expression of wdbGS9548 under the control of Scer\GAL4arm.PS rescues lethality in 52% of Pten3/Df(2L)flp170B animals.