Deletion that removes the majority of the CLIP-190 gene, including the CAP-Gly domain (nucleotides 2L:17389389..17406580 , release 5 genome, have been removed).
A deletion generated by homologous recombination of the region 2L:17389389..17406580 (R5 coordinates).
The length of the motor nerves is normal in stage 16 CLIP-190KO/Df(2L)CLIP-190 embryos (also carrying Rpb11Ubi.PB to rescue the loss of Rpb11 function in Df(2L)CLIP-190). There are no obvious changes in general morphology or overall terminal length at the neuromuscular junction of late third instar larvae.
Cultured primary neurons derived from homozygous CLIP-190KO embryos have a normal axon length compared to wild-type controls.
CLIP-190KO/CLIP-190KO is a non-suppressor of axon phenotype of chb2
CLIP-190KO/CLIP-190KO is a non-suppressor of axon phenotype of Apc2g10, ApcQ8
CLIP-190KO/CLIP-190KO is a non-suppressor of axon phenotype of shot3
CLIP-190KO/CLIP-190KO is a non-suppressor of axon phenotype of DCTN1-p150Δ22
The reduction in axon length seen in cultured primary neurons derived from either homozygous chb2 or shot3 embryos is unchanged if the embryos are also homozygous for 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.
Cultured primary neurons derived from doubly homozygous Apc2g10/Apc2g10 ; ApcQ8/ApcQ8 embryos have a significantly increased axon length compared to wild-type controls. This phenotype is unaffected if the embryos are also homozygous for CLIP-190KO.