Allele Dmel\GluRIIA^SP16

General Information
Symbol	Dmel\GluRIIA^SP16	Species	D. melanogaster
Name		FlyBase ID	FBal0085982
Feature type	allele	Associated gene	Dmel\GluRIIA
Also Known As	GluRIIA^A22

Allele class	loss of function allele
Mutagen	P-element activity
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	loss of function allele (Petersen et al., 1997)
Mutagen	P-element activity (Petersen et al., 1997)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	P{lacW}228 (Petersen et al., 1997)
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. (Petersen et al., 1997)
Cytology
Phenotypic Data
Phenotypic Class
	neuroanatomy defective (Petersen et al., 1997) neurophysiology defective (Albin and Davis, 2004, Müller et al., 2011, Marie et al., 2010) neurophysiology defective (with Df(2L)cl-h4) (Davis et al., 1998, Haghighi et al., 2003, Tsurudome et al., 2010) neurophysiology defective \| recessive \| third instar larval stage (Frank et al., 2009) viable (DiAntonio et al., 1999)
Phenotype Manifest In
	bouton (Petersen et al., 1997) embryonic/larval neuromuscular junction (Frank et al., 2009) neuromuscular junction (Marie et al., 2010) synapse (Petersen et al., 1997) synaptic vesicle (Petersen et al., 1997) t-bar (with Df(2L)cl-h4) (Haghighi et al., 2003)
Detailed Description
	Statement Reference GluRIIA[SP16] 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. (Müller et al., 2011) GluRIIA[SP16] mutants exhibit a significant decrease in the amplitude of spontaneous mEPSPs and a corresponding increase in presynaptic vesicle release (quantal content). (Marie et al., 2010) In GluRIIA[SP16]/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). (Tsurudome et al., 2010) In GluRIIA[SP16] 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 GluRIIA[SP16] mutant background is significantly more sensitive to extracellular application of Cd[2+] or Ni[2+] than is the wild-type NMJ. (Frank et al., 2009) The synapse in GluRIIA^SP16 mutants is morphologically wild-type, although with a quantal size ~50% that observed in wild-type. GluRIIA^SP16 mutants exhibit a significant increase in quantal content compared to controls, indicating homeostatic compensation. (Albin and Davis, 2004) The neuromuscular junctions of GluRIIA^SP16/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. (Haghighi et al., 2003) GluRIIA^SP16/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. (Davis et al., 1998) 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. (Petersen et al., 1997)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Statement Reference GluRIIA^SP16, Rac1^J11/Rac1[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16, Rho1[+]/Rho1^k02107b has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16, Rho1^72O/Rho1[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by cac^HC129/cac[+] (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Cdc42[+]/Cdc42³ (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Cdc42[+]/Cdc42⁴ (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Eph[+]/Eph^x652 (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Exn[+]/Exn^EY-Δ23 (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-enhanceable by Scer\GAL4^C57/Eph^DN.Scer\UAS (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective phenotype, non-enhanceable by gsb^{491.dsRNA.Scer\UAS}/Scer\GAL4^C57 (Marie et al., 2010)
Suppressed by
Statement Reference Df(2L)SP22, GluRIIA^SP16 has lethal phenotype, suppressible by GluRIIB^+t.cSa (Schmid et al., 2008) Df(2L)SP22, GluRIIA^SP16 has lethal phenotype, suppressible by GluRIIB^{GluRIIA.CTD.T:Avic\GFP-EGFP} (Schmid et al., 2008) Df(2L)SP22, GluRIIA^SP16 has lethal phenotype, suppressible by GluRIIB^{T:Avic\GFP-EGFP} (Schmid et al., 2008) GluRIIA^SP16, gsb[+]/gsb⁰¹¹⁵⁵ has neurophysiology defective phenotype, suppressible by wg^l-12/wg[+] (Marie et al., 2010) GluRIIA^SP16, wg^l-12/wg[+] has neurophysiology defective phenotype, suppressible by gsb[+]/gsb⁰¹¹⁵⁵ (Marie et al., 2010) GluRIIA^SP16/Df(2L)cl-h4 has neurophysiology defective phenotype, suppressible \| partially by CaMKII^{T287D.Scer\UAS}/Scer\GAL4^Mef2.PR (Haghighi et al., 2003) GluRIIA^SP16/Df(2L)cl-h4 has neurophysiology defective phenotype, suppressible \| partially by CaMKII^{T287D.Scer\UAS}/Scer\GAL4^Mhc.PW (Haghighi et al., 2003) GluRIIA^SP16/Df(2L)cl-h4 has neurophysiology defective phenotype, suppressible by Scer\GAL4^BG380/Khc-73^{dsRNA.Scer\UAS} (Tsurudome et al., 2010) GluRIIA^SP16/Df(2L)cl-h4 has neurophysiology defective phenotype, suppressible by Scer\GAL4^BG380/mir-310^{Scer\UAS.cluster} (Tsurudome et al., 2010) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, suppressible \| partially by Eph^x652 (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, suppressible \| partially by Exn^EY01953/Exn[+]/Eph[+]/Eph^x652 (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, suppressible \| partially by Scer\GAL4^elav-C155/Eph^DN.Scer\UAS (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective phenotype, suppressible by gsb[+]/gsb⁰¹¹⁵⁵ (Marie et al., 2010) GluRIIA^SP16 has neurophysiology defective phenotype, suppressible by Scer\GAL4^elav-C155/gsb^{491.dsRNA.Scer\UAS} (Marie et al., 2010) GluRIIA^SP16 has neurophysiology defective phenotype, suppressible by wg^l-12/wg[+] (Marie et al., 2010)
NOT suppressed by
Statement Reference GluRIIA^SP16/Df(2L)cl-h4 has neurophysiology defective phenotype, non-suppressible by Df(2R)KT40 (Tsurudome et al., 2010) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-suppressible by cac^HC129/cac[+] (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-suppressible by Cdc42[+]/Cdc42³ (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-suppressible by Cdc42[+]/Cdc42⁴ (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-suppressible by Eph[+]/Eph^x652 (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-suppressible by Exn[+]/Exn^EY-Δ23 (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-suppressible by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype, non-suppressible by Scer\GAL4^C57/Eph^DN.Scer\UAS (Frank et al., 2009) GluRIIA^SP16 has neurophysiology defective phenotype, non-suppressible by gsb^{491.dsRNA.Scer\UAS}/Scer\GAL4^C57 (Marie et al., 2010)
Enhancer of
Statement Reference GluRIIA^SP16 is an enhancer of neurophysiology defective phenotype of Rab3-GAP^c04953 (Müller et al., 2011)
Other
Statement Reference Cdc42[+]/Cdc42³, Exn^EY01953/Exn[+], GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) Cdc42[+]/Cdc42³, GluRIIA^SP16, cac^S/cac[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) Cdc42[+]/Cdc42⁴, Exn^EY01953/Exn[+], GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) Df(2L)SP22, GluRIIA^SP16 has lethal phenotype (Schmid et al., 2008) Eph^x652, GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) Exn[+]/Exn^unspecified, GluRIIA^SP16, cac^HC129/cac[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) Exn^EY01953, GluRIIA^SP16, cac^S/cac[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) Exn^EY01953, GluRIIA^SP16, Scer\GAL4^elav-C155, cac^{Scer\UAS.T:Avic\GFP-EGFP} has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) Exn^EY01953, GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) Exn^EY-Δ23, GluRIIA^SP16, cac^S/cac[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) GluRIIA[+]/GluRIIA^SP16, Pak⁶ has neurophysiology defective phenotype (Albin and Davis, 2004) GluRIIA^SP16, cac^S/cac[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) GluRIIA^SP16, dysb^e01028 has neurophysiology defective phenotype (Dickman and Davis, 2009) GluRIIA^SP16, Pak[+]/Pak⁶ has neurophysiology defective phenotype (Albin and Davis, 2004) GluRIIA^SP16, Pak³, Pak[+]/Pak⁶ has neurophysiology defective phenotype (Albin and Davis, 2004) GluRIIA^SP16, Rab3^rup has neurophysiology defective phenotype (Müller et al., 2011) GluRIIA^SP16, Rac1^J11/Rac1[+], cac^S/cac[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) GluRIIA^SP16, Rac1^J11/Rac1[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) GluRIIA^SP16, Rho1[+]/Rho1^k02107b has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) GluRIIA^SP16, Rho1^72O/Rho1[+], cac^S/cac[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) GluRIIA^SP16, Rho1^72O/Rho1[+] has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009) GluRIIA^SP16/Df(2L)cl-h4, wit^unspecified has lethal \| larval stage phenotype (Haghighi et al., 2003)
Phenotype Manifest In
NOT Enhanced by
Statement Reference GluRIIA^SP16, Rac1^J11/Rac1[+] has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16, Rho1[+]/Rho1^k02107b has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16, Rho1^72O/Rho1[+] has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-enhanceable by cac^HC129/cac[+] (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Cdc42[+]/Cdc42³ (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Cdc42[+]/Cdc42⁴ (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Eph[+]/Eph^x652 (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Exn[+]/Exn^EY-Δ23 (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Scer\GAL4^C57/Eph^DN.Scer\UAS (Frank et al., 2009) GluRIIA^SP16 has neuromuscular junction phenotype, non-enhanceable by gsb^{491.dsRNA.Scer\UAS}/Scer\GAL4^C57 (Marie et al., 2010)
Suppressed by
Statement Reference GluRIIA^SP16, gsb[+]/gsb⁰¹¹⁵⁵ has neuromuscular junction phenotype, suppressible by wg^l-12/wg[+] (Marie et al., 2010) GluRIIA^SP16, wg^l-12/wg[+] has neuromuscular junction phenotype, suppressible by gsb[+]/gsb⁰¹¹⁵⁵ (Marie et al., 2010) GluRIIA^SP16/Df(2L)cl-h4 has t-bar phenotype, suppressible \| partially by CaMKII^{T287D.Scer\UAS}/Scer\GAL4^Mhc.PW (Haghighi et al., 2003) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, suppressible \| partially by Eph^x652 (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, suppressible \| partially by Exn^EY01953/Exn[+]/Eph[+]/Eph^x652 (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, suppressible \| partially by Scer\GAL4^elav-C155/Eph^DN.Scer\UAS (Frank et al., 2009) GluRIIA^SP16 has neuromuscular junction phenotype, suppressible by gsb[+]/gsb⁰¹¹⁵⁵ (Marie et al., 2010) GluRIIA^SP16 has neuromuscular junction phenotype, suppressible by Scer\GAL4^elav-C155/gsb^{491.dsRNA.Scer\UAS} (Marie et al., 2010) GluRIIA^SP16 has neuromuscular junction phenotype, suppressible by wg^l-12/wg[+] (Marie et al., 2010)
NOT suppressed by
Statement Reference GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-suppressible by cac^HC129/cac[+] (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-suppressible by Cdc42[+]/Cdc42³ (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-suppressible by Cdc42[+]/Cdc42⁴ (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-suppressible by Eph[+]/Eph^x652 (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-suppressible by Exn[+]/Exn^EY-Δ23 (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-suppressible by Exn^EY01953/Exn[+] (Frank et al., 2009) GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype, non-suppressible by Scer\GAL4^C57/Eph^DN.Scer\UAS (Frank et al., 2009) GluRIIA^SP16 has neuromuscular junction phenotype, non-suppressible by gsb^{491.dsRNA.Scer\UAS}/Scer\GAL4^C57 (Marie et al., 2010)
Other
Statement Reference Cdc42[+]/Cdc42³, Exn^EY01953/Exn[+], GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) Cdc42[+]/Cdc42³, GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) Cdc42[+]/Cdc42⁴, Exn^EY01953/Exn[+], GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) Exn[+]/Exn^unspecified, GluRIIA^SP16, cac^HC129/cac[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) Exn^EY01953, GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) Exn^EY01953, GluRIIA^SP16, Scer\GAL4^elav-C155, cac^{Scer\UAS.T:Avic\GFP-EGFP} has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) Exn^EY01953, GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) Exn^EY01953, GluRIIA^SP16 has NMJ bouton phenotype (Frank et al., 2009) Exn^EY-Δ23, GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) Exn^EY-Δ23, GluRIIA^SP16 has NMJ bouton phenotype (Frank et al., 2009) Exn^EY-Δ50, GluRIIA^SP16 has NMJ bouton phenotype (Frank et al., 2009) GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) GluRIIA^SP16, Rac1^J11/Rac1[+], cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) GluRIIA^SP16, Rac1^J11/Rac1[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) GluRIIA^SP16, Rho1[+]/Rho1^k02107b has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) GluRIIA^SP16, Rho1^72O/Rho1[+], cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009) GluRIIA^SP16, Rho1^72O/Rho1[+] has embryonic/larval neuromuscular junction phenotype (Frank et al., 2009)
Additional Comments
Genetic Interactions
Statement Reference GluRIIA[SP16], rab3-GAP[c04953] double mutants exhibit significantly reduces mEPSP amplitudes compared to rab3-GAP[c04953] mutant synapses alone. As a consequence, the mean EPSP amplitude of GluRIIA[SP16], rab3-GAP[c04953] double mutant neuromuscular junctions is significantly smaller than the EPSP amplitude records in rab3-GAP[c04953] mutants alone. Rab3[rup] GluRIIA[SP16] double mutants exhibit a robust, homeostatic increase in transmitter release that is similar to the one found in GluRIIA[SP16] single mutants. (Müller et al., 2011) Expression of gsb[491.dsRNA.Scer\UAS] under the control of Scer\GAL4[elav-C155] in a GluRIIA[SP16] heterozygous background significantly suppresses the homeostatic increase in presynaptic release normally observed in GluRIIA[SP16] mutants. Expression of gsb[491.dsRNA.Scer\UAS] under the control of Scer\GAL4[C57] does not change the synaptic homeostasis found in GluRIIA[SP16] heterozygotes. Expression of gsb[491.dsRNA.Scer\UAS] under the control of Scer\GAL4[elav-C155] in a GluRIIA[SP16] heterozygous background significantly reduces the synaptic depression normally observed in GluRIIA[SP16] mutants. A gsb[01155]/+ heterozygous background significantly suppresses the magnitude of synaptic homeostasis that is expressed in a GluRIIA[SP16] mutant background. Synaptic homeostasis occurs normally in GluRIIA[SP16] mutants harboring a heterozygous wg[l-12] mutation. There is significantly more homeostatic compensation found in wg[l-12]/+ GluRIIA[SP16] ; gsb[01155] compared to wg[l-12]/+ GluRIIA[SP16] mutants. The presence of wg[l-12]/+ restores homeostatic compensation to levels that are statistically the same as those observed in GluRIIA[SP16] single mutants. (Marie et al., 2010) Df(2R)KT40/Df(2R)KT40, GluRIIA[SP16]/Df(2L)cl-h4 double mutants fail to show any increase in quantal content (QC) compared to that in GluRIIA[SP16]/Df(2L)cl-h4 single mutants. Overexpression of mir-310[Scer\UAS.cluster] driven by Scer\GAL4[BG380] leads to strong suppression of the QC phenotype normally seen in GluRIIA[SP16]/Df(2L)cl-h4 mutants. Expression of Khc-73[dsRNA.Scer\UAS] driven by Scer\GAL4[BG380] leads to strong suppression of the QC phenotype normally seen in GluRIIA[SP16]/Df(2L)cl-h4 mutants. (Tsurudome et al., 2010) GluRIIA[SP16] ; dysb[e01028] double mutant larvae do not show homeostatic compensation at the neuromuscular junction. (Dickman and Davis, 2009) In GluRIIA[SP16]; Exn[EY01953] double mutant third instar larvae, similarly to GluRIIA[SP16] single mutants, the spontaneous miniature release amplitude (mepsp) is decreased at the neuromuscular junction (NMJ). However, in contrast to GluRIIA[SP16] single mutants, or GluRIIA[SP16] mutants that also carry the precise excision allele Exn[EY-5], GluRIIA[SP16]; Exn[EY01953] double mutant neuromuscular junctions do not show a corresponding increase in quantal content. GluRIIA[SP16] mutant larvae, also homozygous for either an Exn[EY01953] or an Exn[EY-Δ23] or an Exn[EY-Δ50] allele, show a slight but significant increase in bouton number at the NMJ compared to GluRIIA[SP16] single mutants. GluRIIA[SP16] mutant larvae, also homozygous for either an Exn[EY01953] or an Exn[EY-Δ23] or an Exn[EY-Δ50] allele, show no difference in average active zone number per NMJ compared to GluRIIA[SP16] single mutants. The recessive GluRIIA[SP16] single mutant NMJ synaptic homeostasis phenotype is not enhanced nor suppressed by either the Exn[EY01953] or the Exn[EY-Δ23] heterozygous mutations. The heterozygous cac[S]/+ mutation mildly suppresses, but does not abolish the synaptic homeostatic compensation response at the neuromuscular junction (NMJ) seen in homozygous GluRIIA[SP16] single mutants. The recessive GluRIIA[SP16] single mutant NMJ synaptic homeostatic response is completely suppressed in the presence of a heterozygous cac[S]/+ mutation in combination with either an Exn[EY01953]/+ or an Exn[EY-Δ23]/+ heterozygous genetic background. The presence of the heterozygous cac[HC129]/+ mutation has little effect on the quantal content in a homozygous GluRIIA[SP16] background. The recessive GluRIIA[SP16] single mutant NMJ synaptic homeostatic response is completely suppressed in the presence of a heterozygous cac[HC129]/+ mutation in combination with an Exn[unspecified]/+ heterozygous genetic background. Expression of cac[Scer\UAS.T:Avic\GFP-EGFP] driven by Scer\GAL4[elav-C155] in a GluRIIA[SP16]; Exn[EY01953] double mutant background restores the NMJ synaptic homeostatic response to a significant degree. The Rho1[72O]/+ heterozygous mutation can partially suppress the GluRIIA[SP16] NMJ synaptic homeostatic response. The Rho1[k02107b]/+ heterozygous mutation can partially suppress the GluRIIA[SP16] NMJ synaptic homeostatic response. The Exn[EY01953]/+ heterozygous mutation does not enhance the Rho1[72O]/+, GluRIIA[SP16] double mutant NMJ synaptic homeostasis phenotype. The Exn[EY01953]/+ heterozygous mutation does not enhance the Rho1[k02107b]/+, GluRIIA[SP16] double mutant NMJ synaptic homeostasis phenotype. The Rac1[J11]/+ heterozygous mutation causes a mild suppression of the GluRIIA[SP16] NMJ synaptic homeostatic response. The Exn[EY01953]/+ heterozygous mutation does not enhance the Rac1[J11]/+, GluRIIA[SP16] double mutant NMJ synaptic homeostasis phenotype. The Cdc42[3]/+ heterozygous mutation does not suppress or enhance the GluRIIA[SP16] NMJ synaptic homeostasis phenotype. There is no deficit in synaptic bouton number in Cdc42[3]/+ , GluRIIA[SP16] double mutants, compared to wild-type or GluRIIA[SP16] controls. The Cdc42[4]/+ heterozygous mutation does not suppress or enhance the GluRIIA[SP16] NMJ synaptic homeostasis phenotype. There is no deficit in synaptic bouton number in Cdc42[4]/+ , GluRIIA[SP16] double mutants, compared to wild-type or GluRIIA[SP16] controls. Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc42[3]/+ and Exn[EY01953]/+ in a GluRIIA[SP16] mutant genetic background. There is no deficit in synaptic bouton number in Cdc42[3]/+ , Exn[EY01953]/+, GluRIIA[SP16] triple mutants, compared to wild-type or GluRIIA[SP16] controls. Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc42[4]/+ and Exn[EY01953]/+ in a GluRIIA[SP16] mutant genetic background. The heterozygous cac[S]/+ mutation does not abolish the NMJ synaptic homeostatic response in a GluRIIA[SP16] mutant genetic background. The combination of Rac1[J11]/+ and cac[S]/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIA[SP16] genetic background. The combination of Rho1[72O]/+ and cac[S]/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIA[SP16] genetic background. The combination of Cdc42[3]/+ and cac[S]/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIA[SP16] genetic background. The neuromuscular junction (NMJ) bouton numbers in GluRIIA[SP16]; ;Eph[x652] double mutants are not significantly different from that of the GluRIIA[SP16] single mutant. The spontaneous miniature release event (mepsp) amplitudes are significantly decreased in GluRIIA[SP16]; ;Eph[x652] double mutants compared to Eph[x652] single mutants or wild-type. This double mutant phenotype is similar to the one observed in GluRIIA[SP16] single mutants. The average homeostatic increase in presynaptic release observed in GluRIIA[SP16] single mutants is significantly suppressed in GluRIIA[SP16]; ;Eph[x652] double mutants. Expression of Eph[DN.Scer\UAS] with Scer\GAL4[C57] does not significantly change the GluRIIA[SP16] phenotype involving spontaneous miniature release event (mepsp) amplitudes or quantal content at the neuromuscular junction (NMJ). Expression of Eph[DN.Scer\UAS] with Scer\GAL4[elav-C155] does not significantly change the GluRIIA[SP16] phenotype involving spontaneous miniature release event (mepsp) amplitudes, while it does partially suppress the GluRIIA[SP16] quantal content phenotype at the neuromuscular junction (NMJ). The heterozygous Exn[EY01953]/+ mutation alone does not significantly change the recessive GluRIIA[SP16] phenotype involving the synaptic homeostatic compensation at the neuromuscular junction (NMJ). The heterozygous Eph[x652]/+ mutation alone does not significantly change the recessive GluRIIA[SP16] phenotype involving the synaptic homeostatic compensation at the neuromuscular junction (NMJ). The combination of Exn[EY01953]/+ and Eph[x652]/+ heterozygous mutations does not significantly change the GluRIIA[SP16] phenotype involving spontaneous miniature release event (mepsp) amplitudes, while it does partially suppress the GluRIIA[SP16] quantal content phenotype at the neuromuscular junction (NMJ). (Frank et al., 2009) Expression of GluRIIB[T:Avic\GFP-EGFP] rescues the otherwise lethal GluRIIA[SP16]/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics. Co-expression of GluRIIA[T:Avic\GFP-EGFP] and GluRIIB[T:Avic\GFP-EGFP] rescues the otherwise lethal GluRIIA[SP16]/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics. Expression of GluRIIB[+t.cSa] rescues the otherwise lethal GluRIIA[SP16]/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics. Expression of GluRIIB[GluRIIA.CTD.T:Avic\GFP-EGFP] rescues the otherwise lethal GluRIIA[SP16]/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics. (Schmid et al., 2008) Pak⁶/+ ; GluRIIA^SP16/+ mutants do not exhibit a statistically significant decrease in synaptic quantal size compared to wild-type. GluRIIA^SP16; Pak⁶/+ mutants exhibit a statistically significant decrease in synaptic quantal size compared to wild-type. GluRIIA^SP16; Pak⁶/+ mutants exhibit a significant increase in quantal content compared to controls, indicating homeostatic compensation. GluRIIA^SP16; Pak⁶/Pak³ mutants exhibit a statistically significant decrease in synaptic quantal size compared to wild-type. This is a statistically significant decrease compared to GluRIIA^SP16. GluRIIA^SP16; Pak⁶/Pak³ mutants exhibit a significant increase in quantal content compared to controls, indicating homeostatic compensation. (Albin and Davis, 2004) Excitatory postsynaptic potential (EPSP) amplitudes in the neuromuscular junctions of GluRIIA^SP16/Df(2L)cl-h4 larvae are decreased by a third by CaMKII^{T287D.Scer\UAS}; Scer\GAL4^Mef2.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\GAL4^Mhc.PW is used in place of Scer\GAL4^Mef2.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 GluRIIA^SP16/Df(2L)cl-h4 larvae is partially suppressed by CaMKII^{T287D.Scer\UAS}; Scer\GAL4^Mhc.PW. GluRIIA^SP16/Df(2L)cl-h4 ; wit^unspecified/wit^unspecified animal die before the 3rd instar larval stage. (Haghighi et al., 2003) Excitatory postsynaptic potential (EPSP) amplitudes in the neuromuscular junctions of GluRIIA^SP16/Df(2L)cl-h4 larvae are decreased by a third by CaMKII^{T287D.Scer\UAS}; Scer\GAL4^Mef2.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\GAL4^Mhc.PW is used in place of Scer\GAL4^Mef2.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 GluRIIA^SP16/Df(2L)cl-h4 larvae is partially suppressed by CaMKII^{T287D.Scer\UAS}; Scer\GAL4^Mhc.PW. GluRIIA^SP16/Df(2L)cl-h4; wit^unspecified/wit^unspecified animals die before the 3rd instar larval stage. (Haghighi et al., 2003)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	GluRIIA^SP16/Df(2L)SP22 is rescued by GluRIIA^+t.cSa (Schmid et al., 2008) GluRIIA^SP16/Df(2L)SP22 is rescued by GluRIIA^{GluRIIB.CTD.T:Avic\GFP-EGFP} (Schmid et al., 2008) GluRIIA^SP16/Df(2L)SP22 is rescued by GluRIIA^{T:Avic\GFP-EGFP} (Schmid et al., 2008) GluRIIA^SP16 is rescued by GluRIIA^+tg (Petersen et al., 1997) GluRIIA^SP16 is rescued by GluRIIA^Mhc.PP (Petersen et al., 1997)
Comments	Expression of GluRIIA[GluRIIB.CTD.T:Avic\GFP-EGFP] rescues the otherwise lethal GluRIIA[SP16]/Df(2L)SP22 mutant and restores large evoked junctional currents with slow decay kinetics. (Schmid et al., 2008)
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	Null allele. (Petersen et al., 1997)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 5 )
Reported As
Symbol Synonym	df(2L)GluRIIA (Schmid et al., 2008) GluRIIA^A22 (Sigrist et al., 2002, Schmid et al., 2008) Glu-RIIA^SP16 (Haghighi et al., 2003) GluRIIA^SP16 (Frank et al., 2009, Dickman and Davis, 2009, Tsurudome et al., 2010, Müller et al., 2011) GluRIIA^sp16 (Marie et al., 2010)
Name Synonym
Secondary FlyBase IDs

References ( 12 )
Research paper	Müller et al., 2011, Neuron 69(4): 749--762 Rab3-GAP Controls the Progression of Synaptic Homeostasis at a Late Stage of Vesicle Release. [FBrf0213055] Marie et al., 2010, J. Neurosci. 30(24): 8071--8082 Synaptic homeostasis is consolidated by the cell fate gene gooseberry, a Drosophila pax3/7 homolog. [FBrf0211066] Tsurudome et al., 2010, Neuron 68(5): 879--893 The Drosophila miR-310 Cluster Negatively Regulates Synaptic Strength at the Neuromuscular Junction. [FBrf0212495] Dickman and Davis, 2009, Science 326(5956): 1127--1130 The schizophrenia susceptibility gene dysbindin controls synaptic homeostasis. [FBrf0209454] Frank et al., 2009, Neuron 61(4): 556--569 A presynaptic homeostatic signaling system composed of the Eph receptor, ephexin, Cdc42, and CaV2.1 calcium channels. [FBrf0207531] Schmid et al., 2008, Nat. Neurosci. 11(6): 659--666 Activity-dependent site-specific changes of glutamate receptor composition in vivo. [FBrf0204865] Albin and Davis, 2004, J. Neurosci. 24(31): 6871--6879 Coordinating structural and functional synapse development: postsynaptic p21-activated kinase independently specifies glutamate receptor abundance and postsynaptic morphology. [FBrf0180421] Haghighi et al., 2003, Neuron 39(2): 255--267 Retrograde control of synaptic transmission by postsynaptic CaMKII at the Drosophila neuromuscular junction. [FBrf0160587] Sigrist et al., 2002, J. Neurosci. 22(17): 7362--7372 The postsynaptic glutamate receptor subunit DGluR-IIA mediates long-term plasticity in Drosophila. [FBrf0152143] DiAntonio et al., 1999, J. Neurosci. 19(8): 3023--3032 Glutamate receptor expression regulates quantal size and quantal content at the Drosophila neuromuscular junction. [FBrf0107675] Davis et al., 1998, Neuron 20(2): 305--315 Postsynaptic PKA controls quantal size and reveals a retrograde signal that regulates presynaptic transmitter release in Drosophila. [FBrf0100554] Petersen et al., 1997, Neuron 19(6): 1237--1248 Genetic analysis of glutamate receptors in Drosophila reveals a retrograde signal regulating presynaptic transmitter release. [FBrf0100204]

Allele Dmel\GluRIIASP16

Allele Dmel\GluRIIA^SP16