trnS064117 homozygous embryos have motor axon guidance defects that primarily affect the ISNb and SNa nerves.
Early lethal.
Embryos exhibit occasional dorsalization of LCh5. Transheterozygotes with trnS002405a are semilethal.
trnS064117 has abnormal neuroanatomy | recessive phenotype, enhanceable by caps65.2/caps65.2
caps65.2, trnS064117 has abnormal neuroanatomy | recessive phenotype, suppressible | partially by Scer\GAL4en-e16E/trnUAS.cMa
trnS064117 has larval intersegmental nerve branch ISNb of A1-7 phenotype, enhanceable by caps65.2/caps65.2
trnS064117 has larval segmental nerve branch SNa of A1-7 phenotype, enhanceable by caps65.2/caps65.2
caps65.2, trnS064117 has larval segmental nerve branch SNa of A1-7 phenotype, suppressible | partially by Scer\GAL4en-e16E/trnUAS.cMa
caps65.2, trnS064117 has larval intersegmental nerve branch ISNb of A1-7 phenotype, suppressible | partially by Scer\GAL4en-e16E/trnUAS.cMa
The penetrance of axon guidance defects affecting ISNb and SNa in trnS064117 homozygous embryos is significantly enhanced by caps65.2/caps65.2. In around 20% of these ISNb, a single axon forms a distinctive terminal loop whose distal-most point is at muscle 13. These axon guidance defects are significantly rescued/suppressed by trnScer\UAS.cMa; Scer\GAL4en-e16E.
Δ2-3 induced reversion demonstrates the insertion is responsible for the lethal phenotype.