UASt regulatory sequences drive expression of an inverted repeat.
Expression of Rtnl1GD900 under the control of Scer\GAL4da.G32 results in a more rapid age-progressive decline in climbing abilities of adult flies and mild decrease in their lifespan compared to controls. Expression under the Scer\GAL4RapGAP1-OK6 driver leads to defects in mitochondrial morphology in the distal portions of longer posterior (synapsing at segment 7) motor neuron axons (mitochondria are more elongated), whereas in the shorter anterior axons (synapsing at segment 7) the mitochondrial morphology is comparable to controls.
Expression of Rtnl1GD900 driven by Scer\GAL4elav-C155 (along with UAS-dcr) does not significantly affect quantal content or mini EJP amplitude (1.5 mM Ca[2+]) at the neuromuscular junction of third instar larvae compared to controls.
Expression of Rtnl1GD900 (along with UAS-dcr) driven by Scer\GAL4elav-C155 or Scer\GAL4Mef2.PR or Scer\GAL4Gli.PU (at 0.1 mM Ca[2+]) significantly reduces EJP amplitude at the third instar larval NMJ; reduction in EJP corresponds with a significant decrease in the frequency of successful synaptic transmission.
Expression of Rtnl1GD900 (along with UAS-dcr) driven by Scer\GAL4elav-C155 significantly increases neuromuscular junction bouton number.
Animals expressing Rtnl1GD900 under the control of Scer\GAL4da.G32 show normal climbing ability as early adults, but show a progressive decline in climbing ability as they age.
Epidermal cells in third instar larvae expressing Rtnl1GD900 under the control of Scer\GAL4da.G32 show a striking reorganisation of the endoplasmic reticulum (ER). There is a 3-fold increase in the average length of sheet ER profiles, and denser packing of the ribosome-studded sheet ER. There is a significant increase in the ER stress response in both epidermal cells and cells of the ventral nerve cord in these animals.
Larvae expressing Rtnl1GD900 under the control of Scer\GAL4RapGAP1-OK6 show no defects in mitochondrial number or size in muscle 6/7 neuromuscular junction boutons in anterior abdominal segments. However, in posterior abdominal segments, the boutons of the muscle 6/7 neuromuscular junction contain fewer mitochondria than normal and they are increased in size compared to controls.
Adults expressing Rtnl1GD900 under the control of Scer\GAL4elav.PLu (in the presence of Dcr-2Scer\UAS.cDa to increase the efficiency of RNAi) do not show a significant defect in avoidance of noxious temperature (46[o]C) compared to control flies.
Rtnl1GD900, Scer\GAL4elav-C155 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by atlRNAi.UAS, Scer\GAL4elav-C155
Rtnl1GD900, Scer\GAL4elav-C155 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4elav-C155, atlRNAi.UAS
Rtnl1GD900, Scer\GAL4elav-C155 has NMJ bouton | third instar larval stage phenotype, suppressible by atlRNAi.UAS, Scer\GAL4elav-C155
Rtnl1GD900, Scer\GAL4elav-C155 is a suppressor of NMJ bouton | third instar larval stage phenotype of Scer\GAL4elav-C155, atlRNAi.UAS
ReepA541, ReepB48, Rtnl1GD900, Scer\GAL4tey-5053A has axon | third instar larval stage phenotype
Scer\GAL4tey-5053A>Rtnl1GD900,ReepB48;ReepA541 third instar larvae frequently display gaps in the axonal endoplasmic reticulum (ER), the prevalence of the ER gaps is comparable to that observed in Rtnl11.W,ReepB48;ReepA541 triple mutants.
Co-expression of atldsRNA.Scer\UAS significantly suppresses the increases in neuromuscular junction bouton number seen in Scer\GAL4elav-C155>Rtnl1GD900 third instar larvae (and vice versa).