1bp deletion of nucleotide 162 of the IKKβ cDNA, creating a frameshift mutation that results in a stop codon early in the kinase domain.
Motor neurons in either IKKβCR/IKKβCR or IKKβCR/Df(3R)BSC728 third instar larvae show a decrease in baseline neurotransmission, with mildly reduced mEPSP (mini excitatory postsynaptic potential) and EPSP (excitatory postsynaptic potential) amplitudes, but no change in quantal content compared to controls. IKKβCR/IKKβCR motor neurons display a similar mEPSP frequency as controls.
Motor neurons in IKKβCR/IKKβCR third instar larvae display an increase in both active zone number and density, but a similar number of type I boutons as controls.
IKKβCR has abnormal neurophysiology | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
IKKβCR has abdominal segment motor neuron | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
IKKβCR has embryonic/larval neuromuscular junction | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
Motor neurons in IKKβCR, GluRIIASP16 double mutant third instar larvae have further reduced mEPSP (mini excitatory postsynaptic potential) compared to single IKKβCR (but not GluRIIASP16) mutants; reduced EPSP (excitatory postsynaptic potential) amplitudes compared to either single mutant; and reduced quantal content compared to single GluRIIASP16 (but not IKKβCR) mutants. Their capacity for long-term presynaptic homeostatic plasticity (i.e. increase in quantal content causing an increase in EPSP amplitude, approaching baseline) is completely blocked.