Dominant negative Gl construct.
UASp regulatory sequences drive expression of DCTN1-p150, based on the original DCTN1-p1501 mutation.
Potassium-induced unloading of FM1-43 from neuromuscular junction boutons (pre-loaded into an internalised vesicle population during stimulation) is defective in animals expressing the dominant negative GlΔ.Scer\UAS.P\T under the control of Scer\GAL4VGlut-OK371.
Expression of GlΔ.Scer\UAS.P\T under the control of two copies of Scer\GAL4Act5C results in small, rough eyes with disruptions in the hexagonal packing of the ommatidia.
Cytoplasmic streaming in the oocyte is unaffected by expression of GlΔ.Scer\UAS.P\T under the control of Scer\GAL4nos.UTR.T:Hsim\VP16.
DCTN1-p150Δ.UASp, Scer\GAL4Act5C.PU has visible phenotype, suppressible | partially by spis.UAS, Scer\GAL4Act5C.PU
DCTN1-p150Δ.UASp, Scer\GAL4Act5C.PU has eye phenotype, suppressible | partially by spis.UAS, Scer\GAL4Act5C.PU
DCTN1-p150Δ.UASp, Scer\GAL4Act5C.PU has ommatidium phenotype, suppressible | partially by spis.UAS, Scer\GAL4Act5C.PU
The rough eye phenotype caused by expression of GlΔ.Scer\UAS.P\T under the control of two copies of Scer\GAL4Act5C is significantly suppressed by coexpression of spis.Scer\UAS.