Evidence map›Paper›PMID 25944900›Full record

ArticleThe Journal of biological chemistry2015

Mammalian Target of Rapamycin (mTOR) Tagging Promotes Dendritic Branch Variability through the Capture of Ca2+/Calmodulin-dependent Protein Kinase II α (CaMKIIα) mRNAs by the RNA-binding Protein HuD.

Natasha M Sosanya, Luisa P Cacheaux, Emily R Workman, Farr Niere, Nora I Perrone-Bizzozero, Kimberly F Raab-Graham

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  7. Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021
    Review
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  16. Mechanisms regulating dendritic arbor patterning.Cellular and molecular life sciences : CMLS · 2017
    Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Natasha M SosanyaFrom the Center for Learning and Memory, Department of Neuroscience, Institute for Cell Biology, and United States Army Institute of Surgical Research, Joint Base San Antonio-Fort Sam, Houston, Texas 78234, and.
Luisa P CacheauxFrom the Center for Learning and Memory, Department of Neuroscience.
Emily R WorkmanFrom the Center for Learning and Memory, Department of Neuroscience, Institute for Neuroscience, University of Texas, Austin, Texas 78712.
Farr NiereFrom the Center for Learning and Memory, Department of Neuroscience.
Nora I Perrone-BizzozeroDepartment of Neurosciences, Psychiatry and Behavioral Sciences, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131.
Kimberly F Raab-GrahamFrom the Center for Learning and Memory, Department of Neuroscience, Institute for Cell Biology, and Institute for Neuroscience, University of Texas, Austin, Texas 78712, Kimberly@mail.clm.utexas.edu.
The University of Texas at Austin · USUnited States Army Institute of Surgical Research · USUniversity of New Mexico · US

Funding

Mechanisms of Post-Transcriptional Control of Neuronal mRNAsR01NS030255 · NINDS · UNIVERSITY OF NEW MEXICO · PI PERRONE-BIZZOZERO, NORA IRMA · 1997 to 2011
$2.8M
NIDA NIH HHS DA034897NINDS NIH HHS R01 NS030255NINDS NIH HHS R01 NS30255
6 · The paper itself

Abstract

The fate of a memory, whether stored or forgotten, is determined by the ability of an active or tagged synapse to undergo changes in synaptic efficacy requiring protein synthesis of plasticity-related proteins. A synapse can be tagged, but without the "capture" of plasticity-related proteins, it will not undergo long lasting forms of plasticity (synaptic tagging and capture hypothesis). What the "tag" is and how plasticity-related proteins are captured at tagged synapses are unknown. Ca(2+)/calmodulin-dependent protein kinase II α (CaMKIIα) is critical in learning and memory and is synthesized locally in neuronal dendrites. The mechanistic (mammalian) target of rapamycin (mTOR) is a protein kinase that increases CaMKIIα protein expression; however, the mechanism and site of dendritic expression are unknown. Herein, we show that mTOR activity mediates the branch-specific expression of CaMKIIα, favoring one secondary, daughter branch over the other in a single neuron. mTOR inhibition decreased the dendritic levels of CaMKIIα protein and mRNA by shortening its poly(A) tail. Overexpression of the RNA-stabilizing protein HuD increased CaMKIIα protein levels and preserved its selective expression in one daughter branch over the other when mTOR was inhibited. Unexpectedly, deleting the third RNA recognition motif of HuD, the domain that binds the poly(A) tail, eliminated the branch-specific expression of CaMKIIα when mTOR was active. These results provide a model for one molecular mechanism that may underlie the synaptic tagging and capture hypothesis where mTOR is the tag, preventing deadenylation of CaMKIIα mRNA, whereas HuD captures and promotes its expression in a branch-specific manner.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2DendritesELAV-Like Protein 4ELAV ProteinsHippocampusNeuronsProtein BindingRatsRNA, MessengerSynapsesTOR Serine-Threonine KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, ratElavl4 protein, ratELAV-Like Protein 4ELAV ProteinsmTOR protein, ratRNA, MessengerTOR Serine-Threonine Kinasesdendritic branchfluorescencein situ hybridizationmammalian target of rapamycin (mTOR)mRNA decayneuronprotein synthesisRNA-binding proteinsynaptic tagging and capturetranslational control

Identifiers

PMID25944900
PMCPMC4481233
OpenAlexW1587074729

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.