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General Information
Symbol
Dmel\GluRIIASP16
Species
D. melanogaster
Name
FlyBase ID
FBal0085982
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
GluRIIAA22
Nature of the Allele
Mutations Mapped to the Genome
 
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Location
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Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Large portion of the extracellular domain of the GluRIIA gene has been deleted by removal of the 5' 1kb of coding region, plus 8kb of 5' flanking region.

Expression Data
Reporter Expression
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Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
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Motor neurons in GluRIIASP16/GluRIIASP16

third instar larvae show a significant decrease in mEPSP (mini excitatory postsynaptic potential) amplitude leading to significant homeostatic compensatory increases in quantal content compared to controls.

Neurotransmission across the neuromuscular junctions of GluRIIASP16 third instar larvae shows a decrease in mEPSP amplitudes and an increase in quantal content, as compared to controls.

The neurotransmission across the neuromuscular junctions of GluRIIASP16 homozygous mutant wandering third instar larvae exhibits a significant decrease in the amplitude of spontaneous miniature excitatory postsynaptic potential and a significant increase in quantal content, as compared to controls.

GluRIIASP16 homozygous larval neuromuscular junction synapses display both a severe decrease in miniature excitatory postsynaptic potential and a severe increase in quantal content under 0.4mM extracellular Ca[2+] concentration conditions, and both a significant decrease in evoked excitatory postsynaptic potential and a significant increase in readily releasable pool under 3mM extracellular Ca[2+] concentration conditions, as compared to controls. The sucrose-sensitive synaptic vesicle pool (in the absence of extracellular calcium) is not significantly altered compared to controls.

Neurotransmission across GluRIIASP16 larval neuromuscular junctions shows a significant increase in quantal content, as compared to controls.

GluRIIASP16 mutants display reduced amplitude of spontaneous activity events monitored by the Avic\GFPSynapGCaMP6f.Mhc sensor at both motor neuron (MN) Ib and motor neuron Is neuromuscular junctions (NMJs), quantal analysis of basal transmission under low frequency MN stimulation from both inputs shows no difference in normalized release probability or the density of active synapses between the mutants and wild-type controls. However, GluRIIASP16 show significantly higher quantal density per stimulus and single synapse release probability in the Ib input, while no such phenotype is observed in the Is input. The release probability of Is synapse does not seem to be influenced by the synapse's distance to the nearest Ib synapse.

The quantal density depression at the Is input is normal in the mutant NMJs, however Ib inputs show significantly less global facilitation in quantal density during stimulation at 5Hz due to reduction in the number of silent sites recruited during the stimulation train.

GluRIIASP16/Df(2L)cl-h4 mutant larval neuromuscular junctions exhibit decreased amplitude of miniature excitatory junction currents (mEJCs) as compared to controls, no significant difference in EJC amplitude, and quantal content is increased, as compared to controls.

GluRIIASP16/GluRIIASP16 third instar larvae have significantly diminished miniature excitatory postsynaptic potential (mEPSP) amplitudes (decreased quantal size), leading to significant homeostatic compensatory increases in quantal content at the neuromuscular junction (NMJ) compared to controls.

GluRIIASP16/GluRIIASP16 third instar larvae significantly deplete evoked responses over the course of a lengthy high frequency stimulus paradigm (10Hz X 6000 pulses = 10 minutes) in high extracellular calcium (2mM) at the NMJ.

GluRIIASP16 induces a marked decrease in quantal size and an compensatory increase in quantal content compared to wild type.

Third instar larval neuromuscular junctions of GluRIIASP16 homozygous mutants present a significant decrease in spontaneous miniature excitatory postsynaptic potential and a significant increase in quantal content, as compared to controls.

GluRIIASP16/GluRIIASP16 third instar larvae have significantly reduced mEPSP amplitudes and frequency and reduced EPSP amplitude, leading to significant homeostatic compensatory increases in quantal content at the NMJ compared to controls.

GluRIIASP16/Df(2L)cl-h4 mutants show a significant reduction in bouton number at muscle 4 compared to controls. No significant difference is seen in muscle 6/7 NMJs.

GluRIIASP16 mutants exhibit a significant decrease in mEPSP amplitude compared to wild-type. This decrease in mEPSP amplitude is offset by a pronounced increase in quantal content that restores EPSP amplitudes to wild-type values.

GluRIIASP16 mutants exhibit a significant decrease in the amplitude of spontaneous mEPSPs and a corresponding increase in presynaptic vesicle release (quantal content).

In GluRIIASP16/Df(2L)cl-h4 mutant larvae the average amplitude of postsynaptic miniature potentials (mEPJs) and currents (mEJCs) is greatly reduced, but evoked excitatory junctional potentials (EJPs) and evoked excitatory junctional potential currents (EJCs) remain at wild-type levels indicating a large increase in quantal content (QC).

In GluRIIASP16 mutant third instar larvae, the spontaneous miniature release amplitude (mepsp) is significantly decreased, as measured at the neuromuscular junction (NMJ). The decreased mepsp amplitude is partially offset by a homeostatic increase in presynaptic release (quantal content).

Presynaptic release (quantal content) in the GluRIIASP16 mutant background is significantly more sensitive to extracellular application of Cd[2+] or Ni[2+] than is the wild-type NMJ.

The synapse in GluRIIASP16 mutants is morphologically wild-type, although with a quantal size ~50% that observed in wild-type. GluRIIASP16 mutants exhibit a significant increase in quantal content compared to controls, indicating homeostatic compensation.

The neuromuscular junctions of GluRIIASP16/Df(2L)cl-h4 larvae show a significant reduction in quantal size but have excitatory postsynaptic potential (EPSP) amplitudes similar to those of wild-type larvae. (Data from electrophysiological recordings made from muscle 6 in segment A3 of wandering 3rd instar larvae). The neuromuscular junctions of these larvae show a major increase in the number of t-bars per active zone without any gross changes in the overall ultrastructure.

GluRIIASP16/Df(2L)cl-h4 larvae carrying GluRIIB+tg have a 60% reduction in baseline miniature excitatory junctional current amplitude at the neuromuscular junction compared to wild-type, and the time constant of miniature excitatory junctional potential decay is significantly faster than in control larvae.

Shows no obvious behavioral phenotype. Heterozygotes with Df(2L)cl-h4 show large decrease in quantal size, as recorded in muscle 6, segment A3 of female third instar larvae. There is no change in evoked release, indicating a compensatory increase in number of vesicles released, i.e. in quantal content. This is confirmed by failure analysis, using reduced external calcium concentrations. There is a small but significant decrease in bouton number on muscles 6 and 7 in the mutant. The up-regulation of transmitter release is observed over a range of calcium concentrations. Short-term facilitation is not altered at 10Hz or 20Hz.

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Phenotypic Class
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GluRIIASP16, cacS/cac[+] has neurophysiology defective phenotype, enhanceable by Csp[+]/CspDG29203

NOT Enhanced by
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Suppressed by
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GluRIIASP16 has neurophysiology defective phenotype, suppressible by gsb[+]/gsb01155

GluRIIASP16 has neurophysiology defective phenotype, suppressible by wgl-12/wg[+]

GluRIIASP16, wgl-12/wg[+] has neurophysiology defective phenotype, suppressible by gsb[+]/gsb01155

GluRIIASP16, gsb[+]/gsb01155 has neurophysiology defective phenotype, suppressible by wgl-12/wg[+]

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Suppressed by
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GluRIIASP16 has neuromuscular junction phenotype, suppressible by gsb[+]/gsb01155

GluRIIASP16 has neuromuscular junction phenotype, suppressible by wgl-12/wg[+]

GluRIIASP16, wgl-12/wg[+] has neuromuscular junction phenotype, suppressible by gsb[+]/gsb01155

GluRIIASP16, gsb[+]/gsb01155 has neuromuscular junction phenotype, suppressible by wgl-12/wg[+]

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Motor neurons in GluRIIASP16 third instar larvae also mutant for imdNP1182, IKKβCR or RelE20 have further reduced mEPSP (mini excitatory postsynaptic potential) compared to single imdNP1182, IKKβCR or RelE20 (but not GluRIIASP16) mutants; reduced EPSP (excitatory postsynaptic potential) amplitudes compared to each single mutant; and reduced quantal content compared to single GluRIIASP16 (but not imdNP1182, IKKβCR or RelE20) 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.

Motor neurons in either Tak12 ; GluRIIASP16 or Tak1179 ; GluRIIASP16 double mutant third instar larvae display characteristics of long-term presynaptic homeostatic plasticity: reduced mEPSP (mini excitatory postsynaptic potential) accompanied by increased quantal content compared to either Tak12 or Tak1179 but not GluRIIASP16 single mutants. Additionally, Tak1179 ; GluRIIASP16 larvae display reduced EPSP amplitudes compared to either single mutant.

PldnΔ1 homozygosity does not significantly affect the decreased amplitude of spontaneous miniature excitatory postsynaptic potentials, the increased quantal content, or the amplitude of evoked excitatory postsynaptic potentials exhibited during the neurotransmission across the neuromuscular junctions of GluRIIASP16 homozygous wandering third instar larvae.

The increased quantal content, but not the decreased miniature excitatory postsynaptic potentials, observed at the larval neuromuscular junction of GluRIIASP16 homozygotes under 0.4mM extracellular Ca[2+] concentration conditions is suppressed by KaiR1DMB01010 homozygosity alone, but not in combination with the expression of KaiR1DScer\UAS.cKa under the control of Scer\GAL4RapGAP1-OK6. Their decreased excitatory postsynaptic current amplitude and increased readily releasable pool under 3mM extracellular Ca[2+] concentration conditions are not suppressed by KaiR1DMB01010 homozygosity alone.

The increased quantal content in the neurotransmission across the larval neuromuscular junctions of either TBPHG2 or GluRIIASP16 is suppressed in the double mutants.

Lrrke03680/Lrrke03680 blocks the increased quantal content seen in GluRIIASP16/Df(2L)cl-h4 mutant larval NMJs, via a decrease in excitatory junction current (EJC) amplitude.

Expression of LrrkVDRC.cUa under the control of Scer\GAL4Mhc.PW, but not Scer\GAL4BG380, blocks the increased quantal content seen in GluRIIASP16/Df(2L)cl-h4 mutant larval NMJs, via a decrease in excitatory junction current (EJC) amplitude.

Third instar larval GluRIIASP16/GluRIIASP16;Cskc04256/Cskc04256 or GluRIIASP16/GluRIIASP16;Cskc04256/Cskj1D8 double mutants show significant decreases in mEPSP (decreasing quantal size) but do not show significant increases in quantal content (as seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ; GluRIIASP16/GluRIIASP16;Cskc04256/Cskc04256 double mutants show diminished evoked muscle excitation compared to GluRIIASP16/GluRIIASP16 larvae. Additional presence Cskj1D8/+ does not alter differences in quantal size and content seen in GluRIIASP16/GluRIIASP16 larvae.

GluRIIASP16/GluRIIASP16;cacS/+ third instar larvae show significant decreases in mEPSP (decreasing quantal size) and partial impairment of compensatory homeostatic increases in quantal content (significantly less quantal content than is seen in GluRIIASP16/GluRIIASP16 mutants alone but significantly more than wild type) at the NMJ. GluRIIASP16/GluRIIASP16 cacS/+ Cskj1D8/+ third instar larvae show significant decreases in mEPSP and quantal content at the NMJ.

GluRIIASP16/GluRIIASP16;Cskc04256/Cskc04256 third instar larvae do not show significant differences in the number of boutons per muscle area at the neuromuscular junction (A2 6/7 and A3 6/7) compared to wild type, though do show a significant decrease at A3 6/7 compared to Cskc04256/Cskc04256 larvae; active zone number is increased (though not significantly) at A3 6/7 in double mutants, compared to GluRIIASP16/GluRIIASP16 larvae.

GluRIIASP16/GluRIIASP16;Cskc04256/Cskc04256 third instar larvae do not deplete evoked responses to the same degree as GluRIIASP16/GluRIIASP16 larvae over the course of a lengthy high frequency stimulus paradigm (10Hz X 6000 pulses = 10 minutes) in high extracellular calcium (2mM) at the NMJ.

Larvae with expression of Src64BUY1332 driven in muscles by Scer\GAL4C57 show significant decreases in mEPSP (decreased quantal size) but do not show significant compensatory homeostatic increases in quantal content (as seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ; when expression is driven neuronally by Scer\GAL4elav-C155 the significant increase in quantal content is still seen.

Larvae with expression of Src42AScer\UAS.cPa driven in muscles by Scer\GAL4C57 (at 18[o]C) show significant decreases in mEPSP (decreased quantal size) but do not show significant compensatory homeostatic increases in quantal content (as seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ. Larvae with expression of Src42AYF.Scer\UAS driven in muscles by Scer\GAL4Mhc.PW (at 18[o]C) show significant decreases in mEPSP (decreased quantal size) but do not show significant compensatory homeostatic increases in quantal content (as seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ; when expression is driven by Scer\GAL4VGlut-OK371 the significant increase in quantal content is still seen.

GluRIIASP16/GluRIIASP16 Cskc04256/Cskc04256 Src42Ak10108/+ third instar larvae show significant decreases in mEPSP (decreased quantal size) but do not show significant compensatory homeostatic increases in quantal content (similar to GluRIIASP16/GluRIIASP16 Cskc04256/Cskc04256 double mutants) at the NMJ.

GluRIIASP16/GluRIIASP16 Cskc04256/Cskj1D8 Src64Bko/+ third instar larvae show significant decreases in mEPSP (decreased quantal size) partially restores significant compensatory homeostatic increases in quantal content (unlike GluRIIASP16/GluRIIASP16 Cskc04256/Cskj1D8 double mutants, which do not show significant increases in quantal content) at the NMJ.

GluRIIASP16/GluRIIASP16 Src64Bko/+ or GluRIIASP16/GluRIIASP16 Src42Ak10108/+ third instar larvae look similar to GluRIIASP16/GluRIIASP16 larvae (significant decreases in mEPSP and compensatory homeostatic increases in quantal content) at the NMJ.

GluRIIASP16/GluRIIASP16;Cskc04256/Cskj1D8 third instar larvae show significant decreases in mEPSP (decreasing quantal size) but do not show significant compensatory homeostatic increases in quantal content (as seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ; additional expression of CskScer\UAS.T:Avic\GFP-YFP driven by Scer\GAL4nau.PM or Scer\GAL4VGlut-OK371 restores phenotypes to those seen in GluRIIASP16/GluRIIASP16 mutants alone.

Larvae with expression of CskGD9345 driven in muscles by Scer\GAL4C57 show significant decreases in mEPSP (decreased quantal size) and attenuation of compensatory homeostatic increases in quantal content (as seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ; when expression is driven neuronally by Scer\GAL4elav-C155 the significant increase in quantal content is similar to that seen in GluRIIASP16/GluRIIASP16 mutants.

Third instar GluRIIASP16/GluRIIASP16 larvae with expression of Fas2EP1462 driven by Scer\GAL4C57 show significant decreases in mEPSP (decreasing quantal size) and show significant (though not complete) impairment of compensatory homeostatic increases in quantal content (compared to quantal content increases seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ; GluRIIASP16/GluRIIASP16 larvae with Fas2EP1462 expression driven by Scer\GAL4elav-C155 show similar decreases in mEPSP and increases in quantal content as GluRIIASP16/GluRIIASP16 mutants alone.

Third instar GluRIIASP16/GluRIIASP16 larvae with co-expression of Fas2EP1462 and CskScer\UAS.T:Avic\GFP-YFP driven by Scer\GAL4C57 show significant decreases in mEPSP (decreasing quantal size) and show complete impairment of compensatory homeostatic increases in quantal content (compared to significant quantal content increases seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ.

GluRIIASP16/GluRIIASP16;Cskc04256/Cskj1D8 third instar larvae show significant decreases in mEPSP (decreasing quantal size) but do not show significant compensatory homeostatic increases in quantal content (as seen in GluRIIASP16/GluRIIASP16 mutants alone) at the NMJ; additional presence of Fas2e76 restores phenotypes to those seen in GluRIIASP16/GluRIIASP16 mutants alone. GluRIIASP16/GluRIIASP16;Cskc04256/Cskj1D8 Fas2e76 third instar larvae also show a small significant increase in bouton number per muscle area (segment A2, synapse 6/7).

Synaptic homeostasis is impaired in the NMJs of GluRIIASP16 CspDG29203 double mutant larvae compared with either mutant alone. The double mutant larvae show the decreased quantal size seen in GluRIIASP16 mutants but the usual compensatory upregulation of quantal content is not seen: quantal content is not increased compared with CspDG29203 mutants alone. As a result, evoked postsynaptic excitation is impaired.

Synaptic homeostasis is impaired in the NMJs of GluRIIASP16; CspEY22488/+ mutant larvae compared with either mutant alone. The double mutant larvae show the decreased quantal size seen in GluRIIASP16 mutants but the usual compensatory upregulation of quantal content is not seen: quantal content is not increased compared with heterozygous CspEY22488 mutants alone. As a result, evoked postsynaptic excitation is impaired.

The NMJs of cacS GluRIIASP16 double mutant larvae exhibit partially impaired synaptic homeostasis.

One copy of CspDG29203 prevents the compensatory increase in quantal content seen in the NMJs of cacS/+; GluRIIASP16 mutant larvae that have reduced quantal size, resulting in impaired evoked neurotransmission. There is no increase in quantal content compared with cacS/+; CspDG29203/+ controls.

One copy of Df(2L)BSC4 partially prevents the compensatory increase in quantal content seen in the NMJs of GluRIIASP16 mutant larvae that have reduced quantal size, resulting in impaired evoked neurotransmission. There is a slight increase in quantal content compared with Df(2L)BSC4/+ controls, but not enough to compensate for the reduced quantal size.

One copy of Plc21CA does not prevent the compensatory increase in quantal content seen in the NMJs GluRIIASP16 mutant larvae that have reduced quantal size. Evoked neurotransmission is therefore unaffected.

One copy of Gαq1370 partially prevents the compensatory increase in quantal content seen in the NMJs of GluRIIASP16 mutant larvae with reduced quantal size, resulting in impaired evoked neurotransmission. These is some increase in quantal content compared with Gαq1370/+ controls, but not enough to compensate for the reduced quantal size.

One copy of Gαqf04219 partially prevents the compensatory increase in quantal content seen in the NMJs of GluRIIASP16 mutant larvae with reduced quantal size, resulting in impaired evoked neurotransmission. These is some increase in quantal content compared with Gαqf04219/+ controls, but not enough to compensate for the reduced quantal size.

One copy of Gαq28 prevents the compensatory increase in quantal content seen in the NMJs of GluRIIASP16 mutant larvae with reduced quantal size, resulting in impaired evoked neurotransmission. There is no increase in quantal content compared with Gαq28/+ controls.

One copy of Gαq221c prevents the compensatory increase in quantal content seen in the NMJs of GluRIIASP16 mutant larvae with reduced quantal size, resulting in impaired evoked neurotransmission. There is no increase in quantal content compared with Gαq221c/+ controls.

PGRP-LCΔE homozygosity reverses the decrease in spontaneous miniature excitatory postsynaptic potential and increase in quantal content observed in the neuromuscular junction of GluRIIASP16 homozygous mutant third instar larvae.

GluRIIASP16/GluRIIASP16;Past160-4/Past1110-1 double mutant larvae show further reductions in mEPSP amplitude compared to Past160-4/Past1110-1 mutants (but similar in amplitude to GluRIIASP16/GluRIIASP16 mutants); the compensation increase in quantal content seen in GluRIIASP16/GluRIIASP16 mutants is not seen in GluRIIASP16/GluRIIASP16;Past160-4/Past1110-1 double mutants (they show similar diminished quantal content as seen in Past160-4/Past1110-1 larvae).

A longer term form of homeostatic compensation triggered at the GluRIIASP16/Df(2L)cl-h4 larval neuromuscular junction (leads to presynaptic increases in quantal content) is defective (no increase in quantal content) in larvae with SmndsRNA.N.Scer\UAS.WIZ driven by Scer\GAL4elav-C155 (but not Scer\GAL4how-24B).

GluRIIASP16, rab3-GAPc04953 double mutants exhibit significantly reduces mEPSP amplitudes compared to rab3-GAPc04953 mutant synapses alone. As a consequence, the mean EPSP amplitude of GluRIIASP16, rab3-GAPc04953 double mutant neuromuscular junctions is significantly smaller than the EPSP amplitude records in rab3-GAPc04953 mutants alone.

Rab3rup GluRIIASP16 double mutants exhibit a robust, homeostatic increase in transmitter release that is similar to the one found in GluRIIASP16 single mutants.

Expression of gsb491.dsRNA.Scer\UAS under the control of Scer\GAL4elav-C155 in a GluRIIASP16 heterozygous background significantly suppresses the homeostatic increase in presynaptic release normally observed in GluRIIASP16 mutants.

Expression of gsb491.dsRNA.Scer\UAS under the control of Scer\GAL4C57 does not change the synaptic homeostasis found in GluRIIASP16 heterozygotes.

Expression of gsb491.dsRNA.Scer\UAS under the control of Scer\GAL4elav-C155 in a GluRIIASP16 heterozygous background significantly reduces the synaptic depression normally observed in GluRIIASP16 mutants.

A gsb01155/+ heterozygous background significantly suppresses the magnitude of synaptic homeostasis that is expressed in a GluRIIASP16 mutant background.

Synaptic homeostasis occurs normally in GluRIIASP16 mutants harboring a heterozygous wgl-12 mutation.

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.

Df(2R)KT40/Df(2R)KT40, GluRIIASP16/Df(2L)cl-h4 double mutants fail to show any increase in quantal content (QC) compared to that in GluRIIASP16/Df(2L)cl-h4 single mutants.

Overexpression of mir-310Scer\UAS.cluster driven by Scer\GAL4BG380 leads to strong suppression of the QC phenotype normally seen in GluRIIASP16/Df(2L)cl-h4 mutants.

Expression of Khc-73dsRNA.Scer\UAS driven by Scer\GAL4BG380 leads to strong suppression of the QC phenotype normally seen in GluRIIASP16/Df(2L)cl-h4 mutants.

GluRIIASP16 ; dysbe01028 double mutant larvae do not show homeostatic compensation at the neuromuscular junction.

In GluRIIASP16; ExnEY01953 double mutant third instar larvae, similarly to GluRIIASP16 single mutants, the spontaneous miniature release amplitude (mepsp) is decreased at the neuromuscular junction (NMJ). However, in contrast to GluRIIASP16 single mutants, or GluRIIASP16 mutants that also carry the precise excision allele ExnEY-5, GluRIIASP16; ExnEY01953 double mutant neuromuscular junctions do not show a corresponding increase in quantal content.

GluRIIASP16 mutant larvae, also homozygous for either an ExnEY01953 or an ExnEY-Δ23 or an ExnEY-Δ50 allele, show a slight but significant increase in bouton number at the NMJ compared to GluRIIASP16 single mutants.

GluRIIASP16 mutant larvae, also homozygous for either an ExnEY01953 or an ExnEY-Δ23 or an ExnEY-Δ50 allele, show no difference in average active zone number per NMJ compared to GluRIIASP16 single mutants.

The recessive GluRIIASP16 single mutant NMJ synaptic homeostasis phenotype is not enhanced nor suppressed by either the ExnEY01953 or the ExnEY-Δ23 heterozygous mutations.

The heterozygous cacS/+ mutation mildly suppresses, but does not abolish the synaptic homeostatic compensation response at the neuromuscular junction (NMJ) seen in homozygous GluRIIASP16 single mutants.

The recessive GluRIIASP16 single mutant NMJ synaptic homeostatic response is completely suppressed in the presence of a heterozygous cacS/+ mutation in combination with either an ExnEY01953/+ or an ExnEY-Δ23/+ heterozygous genetic background.

The presence of the heterozygous cacHC129/+ mutation has little effect on the quantal content in a homozygous GluRIIASP16 background.

The recessive GluRIIASP16 single mutant NMJ synaptic homeostatic response is completely suppressed in the presence of a heterozygous cacHC129/+ mutation in combination with an Exnunspecified/+ heterozygous genetic background.

Expression of cacScer\UAS.T:Avic\GFP-EGFP driven by Scer\GAL4elav-C155 in a GluRIIASP16; ExnEY01953 double mutant background restores the NMJ synaptic homeostatic response to a significant degree.

The Rho172O/+ heterozygous mutation can partially suppress the GluRIIASP16 NMJ synaptic homeostatic response.

The Rho1k02107b/+ heterozygous mutation can partially suppress the GluRIIASP16 NMJ synaptic homeostatic response.

The ExnEY01953/+ heterozygous mutation does not enhance the Rho172O/+, GluRIIASP16 double mutant NMJ synaptic homeostasis phenotype.

The ExnEY01953/+ heterozygous mutation does not enhance the Rho1k02107b/+, GluRIIASP16 double mutant NMJ synaptic homeostasis phenotype.

The Rac1J11/+ heterozygous mutation causes a mild suppression of the GluRIIASP16 NMJ synaptic homeostatic response.

The ExnEY01953/+ heterozygous mutation does not enhance the Rac1J11/+, GluRIIASP16 double mutant NMJ synaptic homeostasis phenotype.

The Cdc423/+ heterozygous mutation does not suppress or enhance the GluRIIASP16 NMJ synaptic homeostasis phenotype. There is no deficit in synaptic bouton number in Cdc423/+ , GluRIIASP16 double mutants, compared to wild-type or GluRIIASP16 controls.

The Cdc424/+ heterozygous mutation does not suppress or enhance the GluRIIASP16 NMJ synaptic homeostasis phenotype. There is no deficit in synaptic bouton number in Cdc424/+ , GluRIIASP16 double mutants, compared to wild-type or GluRIIASP16 controls.

Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc423/+ and ExnEY01953/+ in a GluRIIASP16 mutant genetic background. There is no deficit in synaptic bouton number in Cdc423/+ , ExnEY01953/+, GluRIIASP16 triple mutants, compared to wild-type or GluRIIASP16 controls.

Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc424/+ and ExnEY01953/+ in a GluRIIASP16 mutant genetic background.

The heterozygous cacS/+ mutation does not abolish the NMJ synaptic homeostatic response in a GluRIIASP16 mutant genetic background.

The combination of Rac1J11/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.

The combination of Rho172O/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.

The combination of Cdc423/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.

The neuromuscular junction (NMJ) bouton numbers in GluRIIASP16; ;Ephx652 double mutants are not significantly different from that of the GluRIIASP16 single mutant.

The spontaneous miniature release event (mepsp) amplitudes are significantly decreased in GluRIIASP16; ;Ephx652 double mutants compared to Ephx652 single mutants or wild-type. This double mutant phenotype is similar to the one observed in GluRIIASP16 single mutants.

The average homeostatic increase in presynaptic release observed in GluRIIASP16 single mutants is significantly suppressed in GluRIIASP16; ;Ephx652 double mutants.

Expression of EphDN.Scer\UAS with Scer\GAL4C57 does not significantly change the GluRIIASP16 phenotype involving spontaneous miniature release event (mepsp) amplitudes or quantal content at the neuromuscular junction (NMJ).

Expression of EphDN.Scer\UAS with Scer\GAL4elav-C155 does not significantly change the GluRIIASP16 phenotype involving spontaneous miniature release event (mepsp) amplitudes, while it does partially suppress the GluRIIASP16 quantal content phenotype at the neuromuscular junction (NMJ).

The heterozygous ExnEY01953/+ mutation alone does not significantly change the recessive GluRIIASP16 phenotype involving the synaptic homeostatic compensation at the neuromuscular junction (NMJ).

The heterozygous Ephx652/+ mutation alone does not significantly change the recessive GluRIIASP16 phenotype involving the synaptic homeostatic compensation at the neuromuscular junction (NMJ).

The combination of ExnEY01953/+ and Ephx652/+ heterozygous mutations does not significantly change the GluRIIASP16 phenotype involving spontaneous miniature release event (mepsp) amplitudes, while it does partially suppress the GluRIIASP16 quantal content phenotype at the neuromuscular junction (NMJ).

Expression of GluRIIBT:Avic\GFP-EGFP rescues the otherwise lethal GluRIIASP16/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics.

Co-expression of GluRIIAT:Avic\GFP-EGFP and GluRIIBT:Avic\GFP-EGFP rescues the otherwise lethal GluRIIASP16/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics.

Expression of GluRIIB+t.cSa rescues the otherwise lethal GluRIIASP16/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics.

Expression of GluRIIBGluRIIA.CTD.T:Avic\GFP-EGFP rescues the otherwise lethal GluRIIASP16/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics.

Pak6/+ ; GluRIIASP16/+ mutants do not exhibit a statistically significant decrease in synaptic quantal size compared to wild-type. GluRIIASP16; Pak6/+ mutants exhibit a statistically significant decrease in synaptic quantal size compared to wild-type. GluRIIASP16; Pak6/+ mutants exhibit a significant increase in quantal content compared to controls, indicating homeostatic compensation. GluRIIASP16; Pak6/Pak3 mutants exhibit a statistically significant decrease in synaptic quantal size compared to wild-type. This is a statistically significant decrease compared to GluRIIASP16. GluRIIASP16; Pak6/Pak3 mutants exhibit a significant increase in quantal content compared to controls, indicating homeostatic compensation.

Excitatory postsynaptic potential (EPSP) amplitudes in the neuromuscular junctions of GluRIIASP16/Df(2L)cl-h4 larvae are decreased by a third by CaMKIIT287D.Scer\UAS; Scer\GAL4Mef2.PR, but quantal size is unaffected, resulting in a significant decrease (p < 0.001) in quantal content (a 57% decrease (corrected for nonlinear summation)). Similar results are seen when Scer\GAL4Mhc.PW is used in place of Scer\GAL4Mef2.PR. (Data from electrophysiological recordings made from muscle 6 in segment A3 of wandering 3rd instar larvae). The increase in t-bars per active zone in neuromuscular junctions of GluRIIASP16/Df(2L)cl-h4 larvae is partially suppressed by CaMKIIT287D.Scer\UAS; Scer\GAL4Mhc.PW. GluRIIASP16/Df(2L)cl-h4 ; witunspecified/witunspecified animal die before the 3rd instar larval stage.

Excitatory postsynaptic potential (EPSP) amplitudes in the neuromuscular junctions of GluRIIASP16/Df(2L)cl-h4 larvae are decreased by a third by CaMKIIT287D.Scer\UAS; Scer\GAL4Mef2.PR, but quantal size is unaffected, resulting in a significant decrease in quantal content (a 57% decrease when corrected for nonlinear summation). Similar results are seen when Scer\GAL4Mhc.PW is used in place of Scer\GAL4Mef2.PR. (Data from electrophysiological recordings made from muscle 6 in segment A3 of wandering 3rd instar larvae).

The increase in t-bars per active zone in neuromuscular junctions of GluRIIASP16/Df(2L)cl-h4 larvae is partially suppressed by CaMKIIT287D.Scer\UAS; Scer\GAL4Mhc.PW.

GluRIIASP16/Df(2L)cl-h4; witunspecified/witunspecified animals die before the 3rd instar larval stage.

Xenogenetic Interactions
Statement
Reference

Expression of Hsap\LRRK2G2019S.Scer\UAS, but not Hsap\LRRK2Scer\UAS.cVa, under the control of Scer\GAL4how-24B partially suppresses the increased quantal content observed in GluRIIASP16/Df(2L)cl-h4 mutant larval neuromuscular junctions.

Complementation and Rescue Data
Comments

Expression of GluRIIAGluRIIB.CTD.T:Avic\GFP-EGFP rescues the otherwise lethal GluRIIASP16/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics.

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Comments

Null allele.

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References (32)