A 4bp insertion, GTAC, has been introduced into the Ptpmeg gene. This produces a frameshift, which leads to truncation within the PDZ domain.
axon & ellipsoid body
axon & ellipsoid body (with Df(3L)ED201)
axon & mushroom body | somatic clone | cell non-autonomous
Homozygous Ptpmeg1 causes accelerated migration of border cells during oogenesis.
Ptpmeg1 adults often become trapped alive in their food.
Ptpmeg1 mutants show mushroom lobe defects. The alpha lobes are reduced, appearing thin, short or with a thin tip. In a small proportion of mutants, the alpha lobes are missing altogether. Tthe beta lobes often aberrantly touch the midline or are completely fused with the contralateral beta lobe. These defects are recessive and cell body and dendritic regions of mushroom body neurons appear normal.
An increase in mushroom body defects occurs as development progresses in Ptpmeg1 mutants; from 0% to ~55% in dorsal lobes and from ~10% to ~80% in medial lobes between 48 hours post-pupal formation (PPF) and the adult stage. A similar increase in defects can be observed in Ptpmeg1/Df(3L)ED201 mutants. At 24 hours PPF no significant level of defects can be observed but ~15-20% of dorsal lobes exhibit defects at 36 hours and 48 hours PPF and nearly 50% of mutants show defects by the first day of adulthood. In addition to the reduction in the distal region of dorsal lobes, dots of axonal material can frequently be observed near these regions, suggesting that axons retract in the dorsal lobes of Ptpmeg1/Df(3L)ED201 mutants.
Ptpmeg1 mutant clones containing either 1-10 or 10-50 mutant α/β cells do not show mushroom body axon defects. However, clones containing substantial amounts of Ptpmeg1 brain tissue outside of the mushroom bodies do show mushroom body axon defects.
In Ptpmeg1 mutants, ellipsoid body axons reach the midline but their extension toward ventral regions halts prematurely, leaving an omega-shaped ellipsoid body that is open along its ventral aspect. These ellipsoid body axon defects persist into adulthood and can also be observed in Ptpmeg1/Df(3L)ED201 mutants.
Ptpmeg1 has mushroom body phenotype, suppressible by sccP
Ptpmeg1 has ellipsoid body phenotype, suppressible by sccP
Ptpmeg1 is partially rescued by PtpmegUAS.cWa/Scer\GAL4elav.PLu
Ptpmeg1 is partially rescued by PtpmegΔFERM.UAS/Scer\GAL4elav.PLu
Ptpmeg1 is partially rescued by PtpmegG494A.F494A.UAS/Scer\GAL4elav.PLu
Ptpmeg1/Df(3L)ED201 is partially rescued by PtpmegUAS.cWa/Scer\GAL4elav.PLu
Ptpmeg1 is not rescued by PtpmegUAS.cWa/Scer\GAL4EB1
Ptpmeg1 is not rescued by Scer\GAL4elav.PLu/PtpmegC877S.UAS
Ptpmeg1 is not rescued by Scer\GAL4elav.PLu/PtpmegR883M.UAS
Ptpmeg1 is not rescued by PtpmegY650F.D787A.UAS/Scer\GAL4elav.PLu
Expression of PtpmegScer\UAS.cWa under the control of Scer\GAL4elav.PLu fully rescues the alpha lobe defects and partially rescues the beta lobe defects of Ptpmeg1 homozygotes. Scer\GAL4elav.PLu>PtpmegScer\UAS.cWa expression partially rescues the alpha lobe defects of Ptpmeg1/Df(3L)ED201 mutants.
Expression of PtpmegScer\UAS.cWa under the control of Scer\GAL4elav.PLu rescues the ellipsoid body defects of Ptpmeg1 mutants but expression of this transgene within the ellipsoid body itself, under the control of Scer\GAL4EB1, fails to rescue these defects.
Expression of PtpmegΔFERM.Scer\UAS under the control of Scer\GAL4elav.PLu results in a strong rescue of the ellipsoid body defects of Ptpmeg1 mutants, a rescue of the beta lobe overextension phenotype but no rescue of the alpha lobe reduction.
Expression of PtpmegG494A.F494A.Scer\UAS under the control of Scer\GAL4elav.PLu results in an effective rescue of the ellipsoid body defects of Ptpmeg1 mutants, while the ability of the transgene to rescue mushroom body defects is reduced compared to expression of a wild-type transgene.