Imprecise excision of P{lacW}Ent2P124 resulting in the removal of the first 20 bp of the 5' untranslated region (UTR) of Ent2 as well as 227 bp of the intergenic region between Ent2 and CG9596.
Approximate endpoints of deletion resulting from the imprecise excision of P{lacW}Ent2P124. The deletion is reported as removing the first 20 bases of the Ent2 5'UTR and 227 bp of the intergenic region between Ent2 and CG9596. It is not clear what coordinate was used as the transcription start site.
Ent23 mutants show defects in olfactory based associative learning. The olfactory acuity of Ent23 mutants is unimpaired.
Synaptic strength and plasticity at the neuromuscular junction (NMJ) are impaired in Ent23 third instar larvae. The amplitude of spontaneous miniature excitatory junction potentials (mEJPs) is not significantly different in Ent23 mutants and wild-type controls. The frequency of MEJPs, however, is significantly elevated in Ent23 mutants relative to controls. The amplitude of stimulus evoked excitatory junction potentials (EJPs, reflecting synaptic transmitter release) is significantly increased in Ent23 mutants. Paired-pulse plasticity of Ent23 mutant synapses is impaired, while post-tetanic potentiation is normal.
Calcium influx is elevated in Ent23 mutant motor neurons.
Ent23 has abnormal learning | recessive phenotype, non-enhanceable by AdoR1
Ent23 has abnormal neurophysiology | recessive | third instar larval stage phenotype, suppressible by AdoR1
Ent23 has abnormal learning | recessive phenotype, non-suppressible by AdoR1
Flies homozygous for both Ent23 and AdoR1 are completely viable.
The performance index of Ent23, AdoR1 double mutants in associative learning is not significantly different from the performance indices of either the Ent23 of AdoR1 single mutants.
The synaptic defects observed in either Ent23 or AdoR1 single mutants are suppressed in Ent23, AdoR1 double mutants. EJP amplitudes are not significantly different in the double mutant and wild-type controls. Ent23, AdoR1 double mutants also show normal paired-pulse facilitation and calcium influx.