Insertion in the intron downstream of the translation start codon.
Germ band retraction and dorsal closure defects are seen in 1% of p130CAS1/p130CASNP4466 embryos.
Homozygous embryos show axon guidance defects characteristic of increased fasciculation in the ISNb pathway (56.0% of hemisegments), in the SNa pathway (49.0% of hemisegments) and in the central nervous system (37.7% of hemisegments).
p130CASNP4466/Df(3L)ED201 embryos show axon guidance defects characteristic of increased fasciculation in the ISNb pathway (78.0% of hemisegments), in the SNa pathway (69.6% of hemisegments) and in the central nervous system (47.6% of hemisegments).
Src42AE1/+; p130CASNP4466/Df(3L)Exel6083 mutants are viable.
p130CASNP4466/p130CAS1 is rescued by p130CASUAS.GFP/Scer\GAL4hs.PB
p130CASNP4466/Df(3L)ED201 is partially rescued by p130CASUAS.Tag:MYC/Scer\GAL4NP4466
Expression of p130CASScer\UAS.T:Avic\GFP (under the control of Scer\GAL4hs.PB) completely rescues the embryonic germ band retraction and dorsal closure defects observed in p130CAS1/p130CASNP4466 trans-heterozygotes.