P{PZ} insertion in the promoter region at position -46 relative to the transcription initiation site.
Mutants exhibit occasional duplication of RP2 neurons and frequent loss of U and CQ neurons. Posterior commissures are missing or reduced.
Germline clones produce eggs with patterning defects: mirror image duplication of denticle belts.
GluRIIASP16, gsb[+]/gsb01155 has abnormal neurophysiology phenotype, suppressible by wgl-12/wg[+]
gsb[+]/gsb01155 is a suppressor of abnormal neurophysiology phenotype of GluRIIASP16, wgl-12/wg[+]
gsb[+]/gsb01155 is a suppressor of abnormal neurophysiology phenotype of GluRIIASP16
GluRIIASP16, gsb[+]/gsb01155 has neuromuscular junction phenotype, suppressible by wgl-12/wg[+]
gsb[+]/gsb01155 is a suppressor of neuromuscular junction phenotype of GluRIIASP16, wgl-12/wg[+]
gsb[+]/gsb01155 is a suppressor of neuromuscular junction phenotype of GluRIIASP16
A gsb01155/+ heterozygous background significantly suppresses the magnitude of synaptic homeostasis that is expressed in a GluRIIASP16 mutant background.
There is significantly more homeostatic compensation found in wgl-12/+ GluRIIASP16 ; gsb01155 compared to wgl-12/+ GluRIIASP16 mutants. The presence of wgl-12/+ restores homeostatic compensation to levels that are statistically the same as those observed in GluRIIASP16 single mutants.
A. Spradling.
Separable from: Eip75B01155. Evidence suggests that the "l(2)01155" line contains 2 P{PZ} insertions; one at 75B (P{PZ}Eip75B01155) corresponding to the site of the flanking sequence AQ073261, and one at 60F (P{PZ}gsb01155) which causes a mutation in gsb.
Complements: l(2)0006400064. Complements: Kr00895. Complements: Dll01092. Complements: l(2)0184801848. Complements: l(2)1048103263. Complements: l(2)1048110481. Complements: Krk05826. Complements: mtsk12502. Complements: zipk15609.