Synaptic activity regulated mRNA-silencing<i>foci</i>for the fine tuning of local protein synthesis at the synapse

Pascual, Malena Lucía; Luchelli, Luciana; Habif, Martín; Boccaccio, Graciela Lidia

doi:10.4161/cib.20257

Cited by 21 publications

(18 citation statements)

References 36 publications

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“…Unlike the functional linkage between AMPA receptors and TDP-43, the association between synapsin-I and TDP-43 is absolutely novel and suggests a model where TDP-43 could affect synaptic strength by modulating the expression of both synapsin-I and AMPA receptors [ 69 ] (see Figure 1 ). This hypothesis is supported by other evidences that TDP-43 is present at synapses and controls the local synthesis of synaptic proteins [ 135 , 139 ]. Other recent findings have shown that the lack of TDP-43 could affect synapses and cause locomotor deficits in Drosophila [ 134 , 137 ].…”

Section: Mechanisms Of Spinal Cord Plasticity In Models Of Motoneusupporting

confidence: 71%

Neuroplasticity and Repair in Rodent Neurotoxic Models of Spinal Motoneuron Disease

Gulino

2016

Neural Plasticity

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Retrogradely transported toxins are widely used to set up protocols for selective lesioning of the nervous system. These methods could be collectively named “molecular neurosurgery” because they are able to destroy specific types of neurons by using targeted neurotoxins. Lectins such as ricin, volkensin, or modeccin and neuropeptide- or antibody-conjugated saporin represent the most effective toxins used for neuronal lesioning. Some of these specific neurotoxins could be used to induce selective depletion of spinal motoneurons. In this review, we extensively describe two rodent models of motoneuron degeneration induced by volkensin or cholera toxin-B saporin. In particular, we focus on the possible experimental use of these models to mimic neurodegenerative diseases, to dissect the molecular mechanisms of neuroplastic changes underlying the spontaneous functional recovery after motoneuron death, and finally to test different strategies of neural repair. The potential clinical applications of these approaches are also discussed.

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Section: Mechanisms Of Spinal Cord Plasticity In Models Of Motoneusupporting

confidence: 71%

Neuroplasticity and Repair in Rodent Neurotoxic Models of Spinal Motoneuron Disease

Gulino

2016

Neural Plasticity

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“…For comparison, we simultaneously analyzed the response of the S-foci and FMRP granules, which are linked to synaptic translation. The S-foci are synaptic mRNA-silencing foci that dissolve upon NMDAR stimulation, thus releasing transcripts and allowing their translation, and the FMRP-positive granules disassemble upon mGluR stimulation (Antar et al, 2004;Baez et al, 2011;Pascual et al, 2012;Graber et al, 2013). We found that the SX-bodies, the S-foci and the FMRP granules responded to synaptic stimulation with different patterns.…”

Section: Xrn1 Forms Synaptic Bodies That Are Different From Processinmentioning

confidence: 84%

Synaptic control of mRNA translation by reversible assembly of XRN1 bodies

Luchelli¹,

Thomas²,

Boccaccio³

2015

Journal of Cell Science

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Repression of mRNA translation is linked to the formation of specific cytosolic foci such as stress granules and processing bodies, which store or degrade mRNAs. In neurons, synaptic activity regulates translation at the post-synapse and this is important for plasticity. Nmethyl-D-aspartate (NMDA) receptor stimulation downregulates translation, and we speculate that this is linked to the formation of unknown mRNA-silencing foci. Here, we show that the 59-39 exoribonuclease XRN1 forms discrete clusters associated with the post-synapse that are different from processing bodies or stress granules, and we named them synaptic XRN1 bodies (SX-bodies). Using primary neurons, we found that the SX-bodies respond to synapse stimulation and that their formation correlates inversely with the local translation rate. SX-bodies increase in size and number upon NMDA stimulation, and metabotropic glutamate receptor activation provokes SX-body dissolution, along with increased translation. The response is specific and the previously described Smaug1 foci and FMRP granules show a different response. Finally, XRN1 knockdown impairs the translational repression triggered by NMDA. Collectively, these observations support a role for the SX-bodies in the reversible masking and silencing of mRNAs at the synapse.

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“…TDP-43, an RNA binding protein, dynamically plays a role in synaptic activity (34). It was demonstrated that alteration in TDP-43 regulation in the early phases of development might lead to neurodegeneration (35).…”

Section: Discussionmentioning

confidence: 99%

Do Low Serum UCH-L1 and TDP-43 Levels Indicate Disturbed Ubiquitin- Proteosome System in Autism Spectrum Disorder?

Çetin

Tezdig

Tarakçıoğlu

et al. 2017

Arch Neuropsychiatr

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Synaptic activity regulated mRNA-silencingfocifor the fine tuning of local protein synthesis at the synapse

Cited by 21 publications

References 36 publications

Neuroplasticity and Repair in Rodent Neurotoxic Models of Spinal Motoneuron Disease

Neuroplasticity and Repair in Rodent Neurotoxic Models of Spinal Motoneuron Disease

Synaptic control of mRNA translation by reversible assembly of XRN1 bodies

Do Low Serum UCH-L1 and TDP-43 Levels Indicate Disturbed Ubiquitin- Proteosome System in Autism Spectrum Disorder?

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