Cultured primary neurons derived from homozygous embryos have a significantly increased axon length compared to wild-type controls.
GlG38S/GlΔ22 larvae show normal locomotion.
GlG38S/GlΔ22 third instar larvae have a normal number of synaptic boutons per neuromuscular junction (NMJ) in proximal abdominal segments (A2 and A3) but show a small but significant increase in the number of synaptic boutons per NMJ in distal segments (A5 and A6). The terminal boutons (the distal-most synaptic boutons) are swollen at the mutant NMJ and show an approximately 2-fold increase in bouton volume in distal segments.
GlG38S/GlΔ22 larvae show a significant reduction in the amplitude of the evoked junctional potential (EJP) at the NMJ compared to controls.
GlΔ22/Gll1 and homozygous neuroblasts show centrosome and spindle formation defects. Defects include metaphase neuroblasts with curved spindles, unfocused spindle poles, spindles with one or two unattached centrosomes, spindles in which both centrosomes are attached to the same half-spindle, or occasionally neuroblasts with three or four centrosomes forming bipolar or multipolar spindles.
The mitotic index and metaphase:anaphase ratio are increased in homozygous neuroblasts compared to wild type.
DCTN1-p150G38S/DCTN1-p150Δ22 has phenotype, enhanceable by Khc[+]/Khc8
DCTN1-p150Δ22 has axon phenotype, non-suppressible by CLIP-190KO/CLIP-190KO
The increase in axon length seen in cultured primary neurons derived from homozygous DCTN1-p150Δ22 embryos is unchanged if the embryos are also homozygous for CLIP-190KO.
DCTN1-p150Δ22/DCTN1-p150l1 is rescued by DCTN1-p150CH322-82J07
DCTN1-p150Δ22/DCTN1-p150l1 is partially rescued by DCTN1-p150UAS.cLa/Scer\GAL4T80
Expression of GlScer\UAS.cLa under the control of Scer\GAL4T80 rescues the lethality of Gll1/GlΔ22 animals, although the rescued animals are sterile.
Expression of GlCH322-82J07 fully rescues Gll1/GlΔ22 animals (the rescued animals are viable and fertile).