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1.
Figure 2

Figure 2. Dysbindin is required presynaptically for synaptic homeostasis. From: The Schizophrenia Susceptibility Gene Dysbindin Controls Synaptic Homeostasis.

(A) Mutations in dysbindin block the homeostatic increase in quantal content following PhTx application. Data are normalized to each genotype in the absence of PhTx. (B) Representative traces for data in (A). (C) Precise excision of the e01028 transposon (revertant) restores compensation. Neuronal-specific expression of dysb (with or without a venus tag; c155-GAL4/+; UAS-dysb/+; dysb1) restores compensation. Muscle-specific expression (UAS-dysb/+; mhc-GAL4, dysb1/dysb1) does not. (D) Representative traces for data in (C). (E) Sustained homeostatic compensation is blocked in GluRIIASP16; dysb1 double mutants.

Dion K. Dickman, et al. Science. ;326(5956):1127-1130.
2.
Figure 4

Figure 4. Dysbindin modulates the calcium-dependence of vesicle release. From: The Schizophrenia Susceptibility Gene Dysbindin Controls Synaptic Homeostasis.

(A) Quantal content as a function of extracellular calcium concentration. (B) Enhanced paired-pulse facilitation in dysb1 mutants. (C) Quantal content is increased by neuronal overexpression of dysb (dysb OE; c155-GAL4/Y; UAS-dysb/+). (D) Homeostatic compensation is calculated as in Fig. 1E. Compensation is suppressed in cacS/+ (n=15) compared with wild type (n=25; p<0.001; Student’s t-test) or dysb1/+ (n=17; p<0.001; Student’s t-test) but is not further suppressed in cacS/+; dysb1/+ mutants (n=19; p>0.27; Student’s t-test). (E) Compensation remains blocked when cac is neuronally overexpressed in a dysb1 mutant (n=9, dysb;cac OE; c155-GAL4/Y; UAS-cacGFP/+; dysb1). (F) Quantal content is increased by neuronal overexpression of dysb (n=17, dysb OE; c155-GAL4/Y; UAS-dysb/+; p<0.0002; Student’s t-test) and when dysb is overexpressed in a cacS mutant (n=19, cacS/+; dysb OE; cacS/c155-GAL4; UAS-dysb/+; p<0.006; Student’s t-test).

Dion K. Dickman, et al. Science. ;326(5956):1127-1130.
3.
Figure 1

Figure 1. Electrophysiology-based screen for homeostatic mutations. From: The Schizophrenia Susceptibility Gene Dysbindin Controls Synaptic Homeostasis.

(A) Flow diagram of screen strategy and outcome. (B) Histogram of average mEJP amplitude per genotype after PhTx application. Wild-type average mEJP (blue arrow) and wild-type average mEJP after PhTx application (black arrow) are indicated. (C) Histogram of average EJP amplitudes per genotype after PhTx application. Arrows as in (B). Red columns indicate values greater than 2 standard deviations from the mean. (D,E) Homeostatic increases in quantal content observed in published genetic mutations. Data are normalized to the same genotype without PhTx treatment in D, and to wild-type values in E. Full genotypes, n values, and references are shown in Tables S1,2.

Dion K. Dickman, et al. Science. ;326(5956):1127-1130.
4.
Figure 3

Figure 3. NMJ morphology and Dysbindin localization. From: The Schizophrenia Susceptibility Gene Dysbindin Controls Synaptic Homeostasis.

(A) Wild-type (w1118) and dysb1 mutant NMJs co-immunostained for anti-HRP (red; motoneuron membrane) and anti-DLG (green; postsynaptic muscle membrane). (B) ven-dysb expressed in neurons co-localizes with the synaptic vesicle associated protein synapsin (green). (C) Quantification of bouton number at muscles 4 and 6/7 comparing wild-type (n=19) and dysb (n=17) (p>0.41; Student’s t-test). (D) Quantification of nc82 puncta per NMJ comparing wild-type (n=15) and dysb (n=16) (p>0.97; Student’s t-test). (E) Density of nc82 puncta comparing wild-type (n=15) and dysb (n=16) (p>0.32; Student’s t-test). Scale bar is 5 microns.

Dion K. Dickman, et al. Science. ;326(5956):1127-1130.

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