Imprecise excision of P{RS3}ReepACB-0501-3 results in partial deletion of ReepA ( 2R:22 ,926,462..22,928,140), with a P-element footprint (CATGATGAAATAACA) left at the excision site.
A 1679 bp deletion resulting from the imprecise excision of P{RS3}ReepACB-0501-3 removes part of the ReepA gene. Residual P element sequences (CATGATGAAATAACA) are left at the excision site.
ReepA541 homozygous larvae show increased number and size or ER cisternae in abdominal segment 3 muscles 6 and 7; adults exhibit decreased climbing ability.
ReepA541, ReepA541, ReepB48, ReepB48 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of Rtnl11.W
ReepA541, ReepB48, Rtnl11.W has short lived phenotype
ReepA541, ReepB48, Rtnl11.W has abnormal neuroanatomy | third instar larval stage phenotype
ReepA541, ReepA541, ReepB48, ReepB48 is an enhancer of endoplasmic reticulum | third instar larval stage phenotype of Rtnl11.W
ReepA541, ReepB48, Rtnl11.W has subperineurial glial cell | third instar larval stage phenotype
ReepA541, ReepB48, Rtnl11.W has embryonic/larval wrapping glial cell | third instar larval stage phenotype
ReepA541, ReepB48, Rtnl1GD900, Scer\GAL4tey-5053A has axon | third instar larval stage phenotype
ReepA541, ReepB48, Rtnl1GD900, Scer\GAL4tey-5053A has endoplasmic reticulum | third instar larval stage phenotype
ReepA541, ReepB48 has endoplasmic reticulum | third instar larval stage phenotype
Epidermal cells in third instar larvae mutant for both ReepA541 and ReepB48 display loss of endoplasmic reticulum (ER) network organization with longer ribosome studded sheet profiles, no such defects are observed in either of the single mutants.
Rtnl11.W,ReepB48;ReepA541 triple mutants are viable but survive poorly beyond two weeks of age. The gaps in axonal ER observed in Rtnl11.W mutant third instar larvae become more frequent upon combination with ReepB48 or ReepB48 and ReepA541 together. Rtnl11.W,ReepB48;ReepA541 triple mutant larvae have fewer but enlarged ER tubules in peripheral nerve axons and display large abnormal accumulations of the synaptic vesicle protein Csp in axons suggesting defects in axonal transport. Electron microscopy analysis confirms fragmentation of the ER network in the triple mutant axons but while the gaps in ER are significantly larger compared to controls, their average number across larvae is only slightly and not significantly increased. Rtnl11.W,ReepB48;ReepA541 peripheral nerves also display glial phenotypes: subperineural and wrapping glia exhibit longer ER sheets and the wrapping glia display more extensive wrapping of the axons, sometimes completely ensheathing them.
Scer\GAL4tey-5053A>Rtnl1GD900,ReepB48;ReepA541 third instar larvae frequently display gaps in the axonal ER, the prevalence of the ER gaps is comparable to that observed in Rtnl11.W,ReepB48;ReepA541 triple mutants.
Combination with two copies of Rtnl1+tCH322-124P15 rescues the abnormal accumulations of synaptic vesicle protein Csp, used as a read-out for axonal transport, detected in Rtnl11.W,ReepB48;ReepA541 triple mutant third instar larvae.
