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    Pettem et al. reveal that the neuronal protein MDGA1 suppresses the development of inhibitory synapses by disrupting the interaction between neuroligin-2 and neurexin-1, two synaptic cell adhesion molecules associated with autism and schizophrenia. Cultured hippocampal neurons overexpressing MDGA1 (green) show a reduced density of inhibitory inputs (labeled with vesicular GABA transporter, red) compared with neighboring, untransfected neurons. The dendritic marker MAP2 is labeled blue.
    Image © 2013 Pettem et al.
    See page 321.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Protein family linked to autism suppresses the development of inhibitory synapses.

People & Ideas

Heisenberg is studying how cells’ physical properties drive early developmental events.


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Structural analysis of a complex of tubulin and tubulin tyrosine ligase (TTL) reveals insights into TTL’s enzymatic mechanism, how it discriminates between α- and β-tubulin, and its possible evolutionary origin.

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Analysis of three different Rab-RabGEF pairs reveals that RabGEFs contain the minimal targeting machinery for recruiting Rabs to specific membranes.

Phosphorylation of the DYD motif of myosin VI small insert isoform controls the sustainability of exocytosis by tethering secretory granules to the cortical actin network.

Selective suppression of inhibitory synapses—with no effect on excitatory synapses—results from interaction of the autism- and schizophrenia-associated proteins MDGA1 and neuroligin-2 through effects on the neuroligin–neurexin pathway.

Directional neuronal migration is mediated by a dynamic SDF1a source generated through localized SDF1a expression followed by regulated mRNA and protein turnover.



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