Mutant embryos show defects in the lateral chordotonal organs and the ventral nerve cord.
Smaller number of PNS neurons express 22C10 in homozygous embryos and PNS axons dispay severe defects in growth cone guidance and fasciculation. Most noticeable phenotype is splitting of the intersegmental nerve into two fascicles, the ISN 'loop' phenotype. Defects in the CNS are similar to those observed in the PNS. Numerous muscles are missing, displaced or exhibit aberrant shapes. Embryos also contain many mononucleate myoblasts that fail to fuse into muscle syncytia. Defects also in the visceral and cardiac musculature.
Homozygous embryos exhibit loss of neurons.
I. Kiss.
The P{lacW}SmD3k11803 insertion appears to affect only SmD3 function and not Oda function (despite being within an Oda intron), since the lethality of P{lacW}SmD3k11803 homozygotes is fully rescued by the P{SmD3.+t2.3} construct which contains the complete SmD3 gene. Complements: OdaEP2104.
P{lacW} insertion can be excised and revert the lethal phenotype to wild type.
Precise or near precise excision of the P{lacW} insertion reverts both the lethality and the PNS phenotype, demonstrating the insertion causes the phenotype.