A Coordinated Local Translational Control Point at the Synapse Involving Relief from Silencing and MOV10 Degradation

Banerjee, Sourav; Neveu, Pierre; Kosik, Kenneth S.

doi:10.1016/j.neuron.2009.11.023

Cited by 220 publications

(252 citation statements)

References 48 publications

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“…Mouse as well as rat hippocampal neuron cultures were grown as described previously (Banerjee et al 2009). Briefly, hippocampuses from embryonic day 15 (E15) embryos from timed-pregnant mice (C57BL/6) were dissected, and then dissociated neurons were plated (30 cells/mm 2 ) onto poly-L-lysine (1 mg/mL) coated glass coverslips.…”

Section: Neuronal Culturementioning

confidence: 99%

“…Immunostaining DIV18-21 mouse hippocampal neurons were immunostained as described previously (Banerjee et al 2009). Neurons were stained with antibodies against MIWI (1:300 dilution) and MAP2 (1:1000 dilution; Covance, Clone SMI-52).…”

Section: Neuronal Culturementioning

confidence: 99%

“…In situ hybridization was performed as described previously (Banerjee et al 2009) with minor modifications. Briefly, DIV18-21 cultured hippocampal neurons were hybridized using digoxigenin-labeled (DIG Oligonucleotide Tailing Kit, second generation; Roche) Lock Nucleic Acid (LNA)-based antisense oligonucleotide (Exiqon) as well as sense oligonucleotide probes.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

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Identification of piRNAs in the central nervous system

Lee¹,

Banerjee²,

Zhou³

et al. 2011

RNA

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259

290

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Piwi-interacting RNAs (piRNAs) are small noncoding RNAs generated by a conserved pathway. Their most widely studied function involves restricting transposable elements, particularly in the germline, where piRNAs are highly abundant. Increasingly, another set of piRNAs derived from intergenic regions appears to have a role in the regulation of mRNA from early embryos and gonads. We report a more widespread expression of a limited set of piRNAs and particularly focus on their expression in the hippocampus. Deep sequencing of extracted RNA from the mouse hippocampus revealed a set of small RNAs in the size range of piRNAs. These were confirmed by their presence in the piRNA database as well as coimmunoprecipitation with MIWI. Their expression was validated by Northern blot and in situ hybridization in cultured hippocampal neurons, where signal from one piRNA extended to the dendritic compartment. Antisense suppression of this piRNA suggested a role in spine morphogenesis. Possible targets include genes, which control spine shape by a distinctive mechanism in comparison to microRNAs.

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Section: Neuronal Culturementioning

confidence: 99%

Section: Neuronal Culturementioning

confidence: 99%

Section: In Situ Hybridizationmentioning

confidence: 99%

See 1 more Smart Citation

Identification of piRNAs in the central nervous system

Lee¹,

Banerjee²,

Zhou³

et al. 2011

RNA

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259

290

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“…90 Other prominent examples are of Armitage, whose degradation releases translational repression of CaMKII at Drosophila synapses and MOV10, a RISC protein under activity dependent degradative control by proteosomal machinery, that regulates mRNAs like CaMKII and Lypia1. 49,91 Since the discovery of dendritic translation, understanding the cellular and molecular mechanisms underlying regulation of mRNA transport, localization and local translation has been the primary focus of studies on memory associated synaptic plasticity. Over the past 12 y, a series of papers point to a model in which a component of earlier discussed synaptic tag includes local, self-sustaining switch in conformation of CPEB from one that is predominantly repressive to one that is translationally active.…”

Section: Rna Regulation Is Central To Long-term Memory Formationmentioning

confidence: 99%

Long-term memory consolidation: The role of RNA-binding proteins with prion-like domains

Sudhakaran

Ramaswami

2016

RNA Biology

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Long-term and short-term memories differ primarily in the duration of their retention. At a molecular level, long-term memory (LTM) is distinguished from short-term memory (STM) by its requirement for new gene expression. In addition to transcription (nuclear gene expression) the translation of stored mRNAs is necessary for LTM formation. The mechanisms and functions for temporal and spatial regulation of mRNAs required for LTM is a major contemporary problem, of interest from molecular, cell biological, neurobiological and clinical perspectives. This review discusses primary evidence in support for translational regulatory events involved in LTM and a model in which different phases of translation underlie distinct phases of consolidation of memories. However, it focuses largely on mechanisms of memory persistence and the role of prion-like domains in this defining aspect of long-term memory. We consider primary evidence for the concept that Cytoplasmic Polyadenylation Element Binding (CPEB) protein enables the persistence of formed memories by transforming in prion-like manner from a soluble monomeric state to a self-perpetuating and persistent polymeric translationally active state required for maintaining persistent synaptic plasticity. We further discuss prion-like domains prevalent on several other RNA-binding proteins involved in neuronal translational control underlying LTM. Growing evidence indicates that such RNA regulatory proteins are components of mRNP (RiboNucleoProtein) granules. In these proteins, prion-like domains, being intrinsically disordered, could mediate weak transient interactions that allow the assembly of RNP granules, a source of silenced mRNAs whose translation is necessary for LTM. We consider the structural bases for RNA granules formation as well as functions of disordered domains and discuss how these complicate the interpretation of existing experimental data relevant to general mechanisms by which prion-domain containing RBPs function in synapse specific plasticity underlying LTM.

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“…Recent work on the rat hippocampal neuronal culture renders further support to the idea of accumulation of translation repressors. In hippocampal neurons a negative regulator of translation called Mov10 is degraded by the proteasome in NMDAand activity-dependent manners (Banerjee et al 2009). Mov10 is the mammalian homolog of the Drosophila Armitage.…”

Section: Does the Proteasome Have Local Roles In Synaptic Plasticity?mentioning

confidence: 99%

The ubiquitin-proteasome pathway and synaptic plasticity

Hegde¹

2010

Learn. Mem.

131

123

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Proteolysis by the ubiquitin-proteasome pathway (UPP) has emerged as a new molecular mechanism that controls wideranging functions in the nervous system, including fine-tuning of synaptic connections during development and synaptic plasticity in the adult organism. In the UPP, attachment of a small protein, ubiquitin, tags the substrates for degradation by a multisubunit complex called the proteasome. Linkage of ubiquitin to protein substrates is highly specific and occurs through a series of well-orchestrated enzymatic steps. The UPP regulates neurotransmitter receptors, protein kinases, synaptic proteins, transcription factors, and other molecules critical for synaptic plasticity. Accumulating evidence indicates that the operation of the UPP in neurons is not homogeneous and is subject to tightly managed local regulation in different neuronal subcompartments. Investigations on both invertebrate and vertebrate model systems have revealed local roles for enzymes that attach ubiquitin to substrate proteins, as well as for enzymes that remove ubiquitin from substrates. The proteasome also has been shown to possess disparate functions in different parts of the neuron. Here I give a broad overview of the role of the UPP in synaptic plasticity and highlight the local roles and regulation of the proteolytic pathway in neurons.

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A Coordinated Local Translational Control Point at the Synapse Involving Relief from Silencing and MOV10 Degradation

Cited by 220 publications

References 48 publications

Identification of piRNAs in the central nervous system

Identification of piRNAs in the central nervous system

Long-term memory consolidation: The role of RNA-binding proteins with prion-like domains

The ubiquitin-proteasome pathway and synaptic plasticity

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