14-3-3ε and ζ Regulate Neurogenesis and Differentiation of Neuronal Progenitor Cells in the Developing Brain

Toyo-oka, Kazuhito; Wachi, Tomoka; Hunt, Reid; Baraban, Scott C.; Taya, Shinichiro; Ramshaw, Hayley S.; Kaibuchi, Kozo; Schwarz, Quenten; Lopez, Angel F.; Wynshaw‐Boris, Anthony

doi:10.1523/jneurosci.2513-13.2014

Cited by 103 publications

(102 citation statements)

References 50 publications

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“…However, we found an increase in the levels of δ-catenin in the 14-3-3 FKO mice (Figure 6). This is consistent with a recent study conducted in the neural progenitor cells of 14-3-3 deficient mice and may provide a potential molecular mechanism for 14-3-3-dependent regulation of actin dynamics and dendritic spines in post-mitotic neurons (53). …”

Section: Resultssupporting

confidence: 93%

Inhibition of 14-3-3 Proteins Leads to Schizophrenia-Related Behavioral Phenotypes and Synaptic Defects in Mice

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Qiao

Graham

et al. 2015

Biological Psychiatry

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Background The 14-3-3 family of proteins is implicated in the regulation of several key neuronal processes. Previous human and animal studies have suggested an association between 14-3-3 dysregulation and schizophrenia. Methods We characterized the behavioral and functional changes in the transgenic mice that express an isoform-independent 14-3-3 inhibitor peptide in the brain. Results We have recently shown that the 14-3-3 functional knockout mice (FKO) exhibit impairments in associative learning and memory. Here, we report that these 14-3-3 FKO mice display other behavioral deficits which correspond to the core symptoms of schizophrenia. These behavioral deficits may be attributed to alterations in multiple neurotransmission systems in the 14-3-3 FKO mice. Particularly, inhibition of 14-3-3 proteins results in a reduction of dendritic complexity and spine density in forebrain excitatory neurons, which may underlie the altered synaptic connectivity in the prefrontal cortical synapse of the 14-3-3 FKO mice. At the molecular level, this dendritic spine defect may stem from dysregulated actin dynamics due to a disruption of the 14-3-3-dependent regulation of phosphorylated cofilin. Conclusions Collectively, our data provide a link between 14-3-3 dysfunction, synaptic alterations, and schizophrenia-associated behavioral deficits.

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Section: Resultssupporting

confidence: 93%

Inhibition of 14-3-3 Proteins Leads to Schizophrenia-Related Behavioral Phenotypes and Synaptic Defects in Mice

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Qiao

Graham

et al. 2015

Biological Psychiatry

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“…The database link for eomesodermin homolog isoform 1 in Mus musculus. The pattern of immunostaining we obtained matched that from previous publications describing immunostaining in mouse telencephalon (Avila et al, 2014;Toyo-oka et al, 2014), the immunostaining we obtained with the rabbit polyclonal in this study, and the immunostaining we had obtained from other Tbr2 antibodies in previous publications (Noctor et al, 2008;Cunningham et al, 2013b).…”

Section: Antibody Characterizationsupporting

confidence: 85%

Evolutionary origin of Tbr2‐expressing precursor cells and the subventricular zone in the developing cortex

Martínez‐Cerdeño

Cunningham

Camacho

et al. 2015

J of Comparative Neurology

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The subventricular zone (SVZ) is greatly expanded in primates with gyrencephalic cortices, and is thought to be absent from vertebrates with three-layered, lissencephalic cortices, such as the turtle. Recent work in rodents has shown that Tbr2-expressing neural precursor cells in the SVZ produce excitatory neurons for each cortical layer in the neocortex. Many excitatory neurons are generated through a two-step process in which Pax6-expressing radial glial cells divide in the VZ to produce Tbr2-expressing intermediate progenitor cells, which divide in the SVZ to produce cortical neurons. We investigated the evolutionary origin of SVZ neural precursor cells in the prenatal cerebral cortex by testing for the presence and distribution of Tbr2-expressing cells in the prenatal cortex of reptilian and avian species. We found that mitotic Tbr2+ cells are present in the prenatal cortex of lizard, turtle, chicken and dove. Furthermore, Tbr2+ cells are organized into a distinct SVZ in the DVR of turtle forebrain, and in the cortices of chicken and dove. Our results are consistent with the concept that Tbr2+ neural precursor cells were present in the common ancestor of mammals and reptiles. Our data also suggest that the organizing principle guiding the assembly of Tbr2+ cells into an anatomically distinct SVZ, both developmentally and evolutionarily, may be shared across vertebrates. Finally, our results indicate that Tbr2 expression can be used to test for the presence of a distinct SVZ, and to define the boundaries of the SVZ in developing cortices.

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“…This signal may represent the C-terminal fragment of Ca V 1.2, which functions as a calcium channel associated transcription regulator (Gomez-Ospina et al, 2006). 14-3-3ε, a signaling protein involved in neuronal migration and synaptic plasticity, was diffusely distributed in the cytoplasm both at P0 and P28 in neurons and astrocytes (Toyo-oka et al, 2014) (Figures 2K and 2L). FMRP, a polyribosome-associated RNA-binding protein that regulates translation of a large number of mRNAs (Contractor et al, 2015), was found in puncta, which likely reflect FMRP-associated mRNA granules, in the soma as well as dendrites in pyramidal neurons at P7 and P28 (Figures 2M, 2N and S5D).…”

Section: Resultsmentioning

confidence: 99%

High-Throughput, High-Resolution Mapping of Protein Localization in Mammalian Brain by In Vivo Genome Editing

Mikuni

Nishiyama

Sun

et al. 2016

Cell

187

196

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SUMMARY A scalable and high-throughput method to identify precise subcellular localization of endogenous proteins is essential for integrative understanding of a cell at the molecular level. Here, we developed a simple and generalizable technique to image endogenous proteins with high specificity, resolution and contrast in single cells in mammalian brain tissue. The technique, termed SLENDR, uses in vivo genome editing to insert a sequence encoding an epitope tag or a fluorescent protein to a gene of interest by CRISPR-Cas9-mediated homology-directed repair (HDR). Single-cell, HDR-mediated genome editing was achieved by delivering the editing machinery to dividing neuronal progenitors through in utero electroporation. We demonstrate that SLENDR allows rapid determination of the localization and dynamics of many endogenous proteins in various cell types, regions and ages in the brain. Thus, SLENDR provides a high-throughput platform to map the subcellular localization of endogenous proteins with the resolution of micro- to nanometers in the brain.

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14-3-3ε and ζ Regulate Neurogenesis and Differentiation of Neuronal Progenitor Cells in the Developing Brain

Cited by 103 publications

References 50 publications

Inhibition of 14-3-3 Proteins Leads to Schizophrenia-Related Behavioral Phenotypes and Synaptic Defects in Mice

Inhibition of 14-3-3 Proteins Leads to Schizophrenia-Related Behavioral Phenotypes and Synaptic Defects in Mice

Evolutionary origin of Tbr2‐expressing precursor cells and the subventricular zone in the developing cortex

High-Throughput, High-Resolution Mapping of Protein Localization in Mammalian Brain by In Vivo Genome Editing

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