Exon 4 contains a 50bp deletion and frameshift. Prediction is that a section of the normal protein would be deleted followed by an insertion in the N terminus near the putative ligand-binding region.
Mutants show no detectable NMJ neurotransmission and no spontaneous synaptic currents. Glutamate applied directly to the postsynaptic muscle has no effect. Mutants do have normal excitation-contraction coupling in response to direct muscle stimulation. Homozygous KaiRIA1 embryos, homozygous KaiRIA2 embryos and transheterozygous KaiRIA1/KaiRIA2 embryos have normal gross, epidermal and neuromuscular anatomy but fail to hatch and appear paralysed both within the eggshell and when artificially removed from the eggshell. No peristaltic somatic muscle movements occur. Presynaptic morphology is normal; nerves form normal branches to appropriate muscles.
GluRIID1 has lethal | recessive | embryonic stage phenotype, non-suppressible by GluRIIAMhc.Tag:MYC
GluRIID1 has paralytic | recessive phenotype, non-suppressible by GluRIIAMhc.Tag:MYC
Allelic series: KaiRIA1 = KaiRIA2 > KaiRIAP2 > KaiRIAP5 > KaiRIAP1. No KaiRIA is detectable from KaiRIA1 mutants. GluRIIA, GluRIIB and GluRIIC subunits are undetecteable at the KaiRIA1 mutant boutons.