Deflationary tactics with the archive of life: contemporary Jewish art and popular culture

This paper discusses art works by Suzanne Treister, Deborah Kass and Doug Fishbone. It considers the importance of their work for contemporary Jewish identity within the terms of wider conceptual questions that preoccupy contemporary art. These concerns are challenging the perceived structures of power, the “performance” of subjectivity and the questioning of authenticity. A deflationary aesthetic is central to the critique of these structures of thinking fuelled by an interest in the relationship between Jewish subjectivity and popular culture that underpins all of these art works. I argue that popular culture plays a key role as a constituting factor in the production of contemporary Anglophone subjectivity. I use the case studies to develop the argument in the three artists’ specificities and the way they all question the idea of authenticity as a stable source of self-understanding. Suzanne Treister questions history and our relationship with historical events, specifically the Holocaust. She also explores questions of the relationship between structures of power and narratives of history. Debora Kass considers the representation of Jewish women, power and iconicity. Doug Fishbone, a younger artist, takes on self-hate as a transformative tool and as a motif that destabilizes Jewishness as a category, especially in an age of the accelerated post-internet-derived subjectivity

Dapper Antagonist of Catenin-1 Cooperates with Dishevelled-1 during Postsynaptic Development in Mouse Forebrain GABAergic Interneurons

<div><p>Synaptogenesis has been extensively studied along with dendritic spine development in glutamatergic pyramidal neurons, however synapse development in cortical interneurons, which are largely aspiny, is comparatively less well understood. Dact1, one of 3 paralogous Dact (Dapper/Frodo) family members in mammals, is a scaffold protein implicated in both the Wnt/β-catenin and the Wnt/Planar Cell Polarity pathways. We show here that Dact1 is expressed in immature cortical interneurons. Although Dact1 is first expressed in interneuron precursors during proliferative and migratory stages, constitutive <i>Dact1</i> mutant mice have no major defects in numbers or migration of these neurons. However, cultured cortical interneurons derived from these mice have reduced numbers of excitatory synapses on their dendrites. We selectively eliminated Dact1 from mouse cortical interneurons using a conditional knock-out strategy with a Dlx-I12b enhancer-Cre allele, and thereby demonstrate a cell-autonomous role for Dact1 during postsynaptic development. Confirming this cell-autonomous role, we show that synapse numbers in Dact1 deficient cortical interneurons are rescued by virally-mediated re-expression of Dact1 specifically targeted to these cells. Synapse numbers in these neurons are also rescued by similarly targeted expression of the Dact1 binding partner Dishevelled-1, and partially rescued by expression of Disrupted in Schizophrenia-1, a synaptic protein genetically implicated in susceptibility to several major mental illnesses. In sum, our results support a novel cell-autonomous postsynaptic role for Dact1, in cooperation with Dishevelled-1 and possibly Disrupted in Schizophrenia-1, in the formation of synapses on cortical interneuron dendrites.</p></div

Reduction of excitatory synapses in <i>Dact1</i> mutant cortical interneurons is cell-autonomous.

<p>Primary cortical cultures were prepared from postnatal day 0 Interneuron-specific <i>Dact1</i> mutant (<i>IDact1-KO</i>) (right) and control (left) brains, fixed at day <i>in vitro</i> 15, and pre- and post-synaptic co-localized puncta counted along GFP labeled primary dendrites from the cell soma to the first major branch point (arrowheads). VGAT/Gephyrin (inhibitory, <b>A</b>) and Vglut1/PSD95 (excitatory, <b>A</b>') co-localized puncta (arrowheads) along the GFP+ dendrite in control (left) and <i>IDact1-KO</i> (right) mice. Quantification of co-localized inhibitory (<b>B</b>) and excitatory (<b>B</b>') pre- and postsynaptic puncta in control (open bars) and <i>IDact1-KO</i> mutants (closed bars). Data shown are mean ± sem of at least 2 independent experiments, collected from at least 2 mice per genotype, 10–15 neurons per animal. ***<i>p</i><0.001; n.s., not significant. Scale bars = 10 µm.</p

Interneuron-specific expression of Dact1, Dvl1, or DISC1 rescues excitatory synapse numbers in <i>IDact1-KO</i> interneurons.

<p><b>A–B</b> Infected interneurons were detected by expression of mCherry. Characterization of PSD95 puncta on primary dendrites of cultured GFP+ cortical interneurons from control (<b>A</b>) and <i>I-Dact1KO</i> (<b>B</b>) mice infected with IS-lentiviral constructs expressing (<b>i</b>) mCherry alone, (<b>ii</b>) Dact1, (<b>iii</b>) Dvl1, (<b>iv</b>) RacCA, or (<b>v</b>) DISC1. C Quantification of PSD95 puncta per 10 µm of primary dendrite length in control (open bars) and <i>IDact1-KO</i> mutant neurons (closed bars). Results are presented as mean ± sem from at least 2 independent experiments, collected from at least 2 mice per genotype, 10–15 neurons per animal. *<i>p</i><0.05; ***<i>p</i><0.001; n.s., not significant. All <i>p</i> values are relative to either control (IS-lentivirus, none) or <i>IDact1-KO</i> (IS-lentivirus, none). Scale bars = 10 µm.</p

<i>Dact1^−/−</i> mice have no major defects in the migratory paths of ganglionic eminence-derived GABAergic interneurons.

<p><i>In situ</i> hybridization (Lhx6) in rostral to caudal coronal sections through E12.5 (<b>A</b>), E14.5 (<b>A</b>'), and E18.5 (<b>A</b>″) <i>Dact1^−/−</i> brains (bottom) compared to wild type (top). Arrowheads indicate Lhx6 expression in the subventricular zone (closed) and marginal zone (open) of the cortex. <i>In situ</i> hybridization (Dlx1) in E12.5 (<b>B</b>), E14.5 (<b>B</b>'), and E18.5 (<b>B</b>″) <i>Dact1^−/−</i> mice (bottom) compared to wild type (top). cpu, caudate-putamen; cp, cortical plate; hip, hippocampus; lge, lateral ganglionic eminence; mge, medial ganglionic eminence; NAcc, nucleus accumbens; poa, preoptic area; se, septum; st, striatum; vp, ventral pallidum. Scale bars = 500 µm.</p

Cortical interneurons from constitutive <i>Dact1</i> mutant mice have fewer excitatory synapses on primary dendrites.

<p>Primary cortical cultures were prepared from postnatal day 0 <i>Dact1^−/−;Lhx6GFP</i> (right) and control (left) brains, fixed at day <i>in vitro</i> 15, and synaptic puncta counted along GFP labeled primary dendrites from the cell soma to the first major branch point (arrowheads). Inhibitory synaptic puncta were visualized using antibodies against VGAT (presynaptic, <b>A</b>) and Gephyrin (postsynaptic, <b>B</b>) with each marker counted irrespective of co-localization with the other; <b>C</b> Quantification per 10 µm of primary dendrite length in control (open bars) and constitutive <i>Dact1</i> mutant neurons (closed bars). Excitatory synaptic puncta were visualized using antibodies against VGLUT1 (presynaptic, <b>D</b>) and PSD95 (postsynaptic, <b>E</b>) with each marker counted irrespective of co-localization with the other; <b>F</b> Quantification per 10 µm of primary dendrite length. Data shown are mean ± sem of at least 3 independent experiments, collected from at least 3 mice per genotype, 10–15 neurons per animal. **<i>p</i><0.01; ***<i>p</i><0.001; n.s., not significant. Scale bars = 10 µm.</p

<i>Dact1</i> expression in the developing forebrain.

<p><i>In situ</i> hybridization (Dact1) in rostral to caudal coronal sections through wild type E14.5 (<b>A</b>) and E18.5 brains (<b>A</b>'). Arrowheads in <b>A</b> indicate <i>Dact1</i> expression in the deep migratory stream (subventricular zone/intermediate zone) of ganglionic eminence-derived interneurons within the developing cortex. <i>In situ</i> hybridization (Dact1) at E14.5. <b>B </b><i>Dact1</i> expression in <i>Dlx1^−/−;Dlx2^−/−</i> mice (bottom) compared to wild type (top) and higher magnification (<b>B</b>'), shows the absence (closed arrowheads) of <i>Dact1</i> expression in <i>Dlx1^−/−;Dlx2^−/−</i> mutants in the usual position of the deep migratory stream, indicating that Dact1 is normally expressed in the immature interneurons that fail to migrate in this <i>Dlx</i> double mutant. Asterisks in <b>B</b>' indicate the shift in Dact1 mRNA expression from the subventricular zone to the ventricular zone of the ganglionic eminences in <i>Dlx1^−/−;Dlx2^−/−</i> mice. <i>Dact1</i> remains expressed in the marginal zone of the cortex in the double mutants (open arrowheads), reflecting Dlx-independent expression in developing excitatory neurons. cpu, caudate-putamen; ctx, cortex; fr ctx, frontal cortex; gp, globus pallidus; hip, hippocampus; sep, septum; svz, subventricular zone. Scale bars = 500 µm.</p

Posterior malformations in Dact1 mutant mice arise through misregulated Vangl2 at the primitive streak

Mice homozygous for mutations in Dact1 (Dpr/Frodo) phenocopy human malformations involving the spine, genitourinary system, and distal digestive tract. We trace this phenotype to disrupted germ layer morphogenesis at the primitive streak (PS). Remarkably, heterozygous mutation of Vangl2, a transmembrane component of the Planar Cell Polarity (PCP) pathway, rescues recessive Dact1 phenotypes, whereas loss of Dact1 reciprocally rescues semidominant Vangl2 phenotypes. We show that Dact1, an intracellular protein, forms a complex with Vangl2. In Dact1 mutants, Vangl2 is increased at the PS where cells ordinarily undergo an epithelial-mesenchymal transition. This is associated with abnormal E-cadherin distribution and changes in biochemical measures of the PCP pathway. We conclude that Dact1 contributes to morphogenesis at the PS by regulating Vangl2 upstream of cell adhesion and the PCP pathway