CPEB-Mediated Cytoplasmic Polyadenylation and the Regulation of Experience-Dependent Translation of α-CaMKII mRNA at Synapses

Wu, Lin; Wells, David G.; Tay, Joyce; Mendis, Duane B.; Abbott, Mary‐Alice; Barnitt, Allan; Quinlan, Elizabeth; Heynen, Arnold J.; Fallon, Justin R.; Richter, Joel D.

doi:10.1016/s0896-6273(00)80630-3

Cited by 459 publications

(407 citation statements)

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“…[40][41][42] Subsequently, enhanced accumulation in levels of specific mRNAs like CaMKII in dendritic spines following neuronal activity and increase in the polyadenylation and translation of stored, partially deadenylated CaMKII mRNA in mammalian synaptosomal preparations, following glutamate stimulation were observed. [43][44][45] Further studies in Aplysia, [46][47][48] Drosophila 49 and mammalian systems 50,51 showed that protein synthesis at synapses was induced by synaptic activity and provided evidence consistent with it being is required for long-term synaptic plasticity.…”

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

confidence: 97%

“…72,73 The most studied, canonical mechanism of translational activation involves the Cytoplasmic Polyadenylation Element Binding (CPEB1) protein and its regulation of CaMKII mRNA. 43,44,74,75 Activity induced translational regulation has been extensively studied in the case of CaMKII mRNA which is one of the most abundant protein in neurons especially enriched in the post synaptic density (PSD). NMDA receptor activation mediated Ca 2C entry leads to phosphorylation of the T286 residue of the pseudosubstrate domain of the a subunit (T287 of b) leading to a Ca 2C independent autonomous state of activity by autophosphorylation.…”

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

confidence: 99%

“…In the PSD, in response to neuronal stimulation, CPEB likely activates translation of CaMKII and similar mRNAs that possess CPEs in their UTRs. 43 It also associates with motor proteins for mRNA transport and has a role in packaging of bound mRNAs to RNP complexes. 129 CPEB initiates polyadenylation induced translation of dormant mRNAs during Xenopus oocyte maturation.…”

Section: Characterization Of Prions and Prion Domainsmentioning

confidence: 99%

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

confidence: 97%

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

confidence: 99%

Section: Characterization Of Prions and Prion Domainsmentioning

confidence: 99%

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

Sudhakaran

Ramaswami

2016

RNA Biology

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“…Four CPEB isoforms are found in the mouse (Theis et al, 2003). One of which, CPEB-1, has been detected at postsynaptic sites of hippocampal neurons and participates in local NMDAR-dependent polyadenylation of αCamKII and other dendritic mRNAs (Huang et al, 2003;Huang et al, 2002;Wells et al, 2001;Wu et al, 1998). Experiments in CPEB-1 deficient mice revealed that synaptic capture of L-LTP was partially affected in those mice (Alarcon et al, 2004).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

Barco

Armentia

Alarcón

2008

Neuroscience & Biobehavioral Reviews

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Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited ten years later, Neuroscience and Biobehavioral Reviews (2008Reviews ( ), doi:10.1016Reviews ( /j.neubiorev.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.A c c e p t e d m a n u s c r i p t A c c e p t e d m a n u s c r i p tThe STC hypothesis revisited 2 Abstract A decade ago, the synaptic tagging hypothesis was proposed to explain how newly synthesized plasticity products can be specifically targeted to active synapses. A growing number of studies have validated the seminal findings that gave rise to this model, as well as contributed to unveil and expand the range of mechanisms underlying late-associativity and neuronal computation.Here, we will review what it was learnt during this past decade regarding the cellular and molecular mechanisms underlying synaptic tagging and synaptic capture. The accumulated experimental evidence has widened the theoretical framework set by the synaptic tagging and capture (STC) model and introduced concepts that were originally considered part of alternative models for explaining synapse-specific LTP. As a result, we believe that the STC model, now improved and expanded with these new ideas and concepts, still represents the most compelling hypothesis to explain late-associativity in synapse-specific plasticity processes. We will also discuss the impact of this model in our view of the integrative capability of neurons and associative learning. wordsKeywords: synaptic plasticity; LTP; associative learning; neuronal computation; synaptic tagging; synaptic capture; metaplasticity A c c e p t e d m a n u s c r i p tThe STC hypothesis revisited 3 Contents

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“…12 This mechanism has also been shown to control poly(A) tail length in mammalian cells. 13,14 Cytoplasmic polyadenylation is mediated by cytoplasmic polyadenylation binding protein (CPEB), which binds to the highly conserved cytoplasmic polyadenylation element (CPE) in the 3 0 UTR of mRNA. 15 Here, we show that CPEB1 and CPEB2 play a role in the translational control of TWIST1 in a CPE-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression

Vislovukh

Meng

et al. 2012

Oncogene

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TWIST1 is a highly conserved basic helix-loop-helix transcription factor that promotes epithelial --mesenchymal transition (EMT). Its misregulation has been observed in various types of tumors. Using the MCF-10A-series of cell lines that recapitulate the early stages of breast cancer formation and EMT, we found TWIST1 to be upregulated during EMT and downregulated early in carcinogenesis. The TWIST1 3 0 UTR contains putative regulatory elements, including miRNA target sites and two cytoplasmic polyadenylation elements (CPE). We found that miR-580, CPEB1, and CPEB2 act as negative regulators of TWIST1 expression in a sequence-specific and additive/cooperative manner.

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CPEB-Mediated Cytoplasmic Polyadenylation and the Regulation of Experience-Dependent Translation of α-CaMKII mRNA at Synapses

Cited by 459 publications

References 58 publications

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

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

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

Translational control of TWIST1 expression in MCF-10A cell lines recapitulating breast cancer progression

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