Essential Role for Synaptopodin in Dendritic Spine Plasticity of the Developing Hippocampus

Zhang, Xiao Lei; Poschel, B. P. H.; Faul, Christian; Upreti, Chirag; Stanton, Patric K.; Mündel, Peter

doi:10.1523/jneurosci.2983-12.2013

Cited by 59 publications

(74 citation statements)

References 37 publications

(2 reference statements)

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“…Actinins interact via the rod region with proteins enriched at excitatory synapses, including synaptopodin (73,74), an F-actin binding protein (75) tightly connected to the spine apparatus (76) in large mushroom spine heads. Therefore, in mature spines, actinins are positioned to participate in the group 1 mGluR-dependent modification of the actin cytoskeleton that may underlie spine shrinkage accompanying long-term depression.…”

Section: Discussionmentioning

confidence: 99%

Actinin-4 Governs Dendritic Spine Dynamics and Promotes Their Remodeling by Metabotropic Glutamate Receptors

Kalinowska

Chávez

Lutzu

et al. 2015

Journal of Biological Chemistry

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Background: Group 1 mGluRs induce dendritic spine remodeling, but the underlying molecular mechanisms remain uncharacterized. Results: ␣-Actinin-4 regulates dendritic protrusion dynamics and morphogenesis and is required for the receptor-induced dynamic remodeling of dendritic protrusions. Conclusion: ␣-Actinin-4 is a novel molecular effector of mGluR-dependent spine remodeling. Significance: mGluR signaling via actinins could contribute to synaptic plasticity and spine dysmorphogenesis in neurodevelopmental disorders.

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Section: Discussionmentioning

confidence: 99%

Actinin-4 Governs Dendritic Spine Dynamics and Promotes Their Remodeling by Metabotropic Glutamate Receptors

Kalinowska

Chávez

Lutzu

et al. 2015

Journal of Biological Chemistry

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“…DDX3 also functions as a cellular signaling factor and contributes to antiviral innate immunity pathways (Soto-Rifo and Ohlmann, 2013;Ariumi, 2014). Although mammalian DDX3 has multiple cellular functions, the role of DDX3 orthologs in translational control is evolutionarily conserved (Soto-Rifo and Ohlmann, 2013;Ariumi, 2014). One such ortholog, yeast Ded1p, is an essential protein that functions as a translation initiation factor that facilitates ribosome scanning of mRNAs (Iost et al, 1999;Yang and Jankowsky, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Mammalian DDX3 also interacts with several initiation factors, such as components of eIF3 and eIF4F, whereby it facilitates 40S ribosome scanning of the 5Ј untranslated region (UTR) of mRNAs and/or promotes 80S ribosome assembly SotoRifo et al, 2012). Several lines of evidence indicate that DDX3 may regulate the translation of selective mRNAs that contain a structured 5Ј UTR (Lai et al, 2008;Soto-Rifo et al, 2012). DDX3 mediates certain cellular functions through its activity in translational control.…”

Section: Introductionmentioning

confidence: 99%

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DDX3 Modulates Neurite Development via Translationally Activating an RNA Regulon Involved in Rac1 Activation

Chen

Tarn

2016

J. Neurosci.

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The RNA helicase DDX3 is a component of neuronal granules, and its gene mutations are linked to intellectual disability (ID). Here we demonstrate that DDX3 depletion in neurons impairs neurite development by downregulating Rac1 level and activation. Moreover, DDX3 activates the translation of functionally coherent mRNAs involved in Rac1 activation including Rac1. Among the DDX3 regulon, Prkaca encodes the catalytic subunit of PKA, a potential activator of Rac1 in neurons. DDX3-modulated PKAc␣ and Rac1 expression tunes the strength of PKA-Rac1 signaling and thereby contributes to neurite outgrowth and dendritic spine formation. Inhibition of DDX3 activity or expression in neonatal mice impaired dendritic outgrowth and spine formation of hippocampal neurons, echoing neuronal deficits underling DDX3 mutation-associated ID. Finally, we provide evidence that DDX3 activates local protein synthesis through a 5Ј UTR-dependent mechanism in neurons. The novel DDX3 regulon may conduct a spatial and temporal control of Rac1 signaling to regulate neurite development.

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“…Actin is a major cytoskeletal protein in neurons, and it is uniformly distributed throughout axons and dendrites (Zhang et al, 2013). The actin can be either stable or dynamic.…”

Section: The Composition Of Intracellular Actinsmentioning

confidence: 99%

Roles of BMP6/7 in Actin Dynamics in Amyloid β-Induced Neurotoxicity

Sun¹,

Zhang²,

Xiao³

2014

PSYCH

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Actin dynamics plays an important role in many physiological functions such as long-term potentiation, neurotransmission, regulatory proteins translocation, ATP cycle, etc. When amyloid β (Aβ)-induced neurotoxicity occurs, the imbalance of actin dynamics leads to dystrophy of dendrites, which is characteristic pathology in Alzheimer's disease (AD). Transient and persistent Aβ neurotoxicity provokes distinct manifestations of actin dynamics and causes opposing effects in AD. It has been shown that bone morphogenetic protein 6/7 (BMP6/7) protects neuronal morphology against Aβ-induced neurotoxicity, and can directly bind to LIM kinase1 (LIMK1), being one part of the upstream regulatory pathway of actin dynamics. This review aims to discuss a potential mechanism of BMPs underlying maintainance of cytoskeletal stabilization in neurite.

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Essential Role for Synaptopodin in Dendritic Spine Plasticity of the Developing Hippocampus

Cited by 59 publications

References 37 publications

Actinin-4 Governs Dendritic Spine Dynamics and Promotes Their Remodeling by Metabotropic Glutamate Receptors

Actinin-4 Governs Dendritic Spine Dynamics and Promotes Their Remodeling by Metabotropic Glutamate Receptors

DDX3 Modulates Neurite Development via Translationally Activating an RNA Regulon Involved in Rac1 Activation

Roles of BMP6/7 in Actin Dynamics in Amyloid β-Induced Neurotoxicity

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