Evidence map›Paper›PMID 20843478›Full record

ArticleNeurobiology of disease2011

The fragile X mental retardation protein developmentally regulates the strength and fidelity of calcium signaling in Drosophila mushroom body neurons.

Charles R Tessier, Kendal Broadie

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Molecular Logic of Synaptic Diversity BetweenbioRxiv : the preprint server for biology · 2023
    Article
  3. Article
  4. Article
  5. Activity-Dependent Remodeling ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  6. Article
  7. Genetic mutations in CaGenes, brain, and behavior · 2019
    Article
  8. Modeling Fragile X Syndrome inFrontiers in molecular neuroscience · 2018
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Charles R TessierDepartment of Biological Sciences, Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, TN 37232, USA.
Kendal Broadie
John F. Kennedy Center for the Performing Arts · US

Funding

Genetic and Developmental Analyses of Fragile X SyndromeR01MH084989 · NIMH · VANDERBILT UNIVERSITY · PI BROADIE, KENDAL · 2009 to 2021
$5.5M
Genetic and Developmental Analyses of Fragile X Mental Retardation ProteinR56MH084989 · NIMH · VANDERBILT UNIVERSITY · PI BROADIE, KENDAL · 2023 to 2023
$516k
NIMH NIH HHS MH084989NIMH NIH HHS R01 MH084989NIMH NIH HHS R56 MH084989
6 · The paper itself

Abstract

Fragile X syndrome (FXS) is a broad-spectrum neurological disorder characterized by hypersensitivity to sensory stimuli, hyperactivity and severe cognitive impairment. FXS is caused by loss of the fragile X mental retardation 1 (FMR1) gene, whose FMRP product regulates mRNA translation downstream of synaptic activity to modulate changes in synaptic architecture, function and plasticity. Null Drosophila FMR1 (dfmr1) mutants exhibit reduced learning and loss of protein synthesis-dependent memory consolidation, which is dependent on the brain mushroom body (MB) learning and memory center. We targeted a transgenic GFP-based calcium reporter to the MB in order to analyze calcium dynamics downstream of neuronal activation. In the dfmr1 null MB, there was significant augmentation of the calcium transients induced by membrane depolarization, as well as elevated release of calcium from intracellular organelle stores. The severity of these calcium signaling defects increased with developmental age, although early stages were characterized by highly variable, low fidelity calcium regulation. At the single neuron level, both calcium transient and calcium store release defects were exhibited by dfmr1 null MB neurons in primary culture. Null dfmr1 mutants exhibit reduced brain mRNA expression of calcium-binding proteins, including calcium buffers calmodulin and calbindin, predicting that the inability to appropriately sequester cytosolic calcium may be the common mechanistic defect causing calcium accumulation following both influx and store release. Changes in the magnitude and fidelity of calcium signals in the absence of dFMRP likely contribute to defects in neuronal structure/function, leading to the hallmark learning and memory dysfunction of FXS.

Indexed as

Drosophila melanogasterAnimalsCalciumCalcium-Binding ProteinsCalcium SignalingCells, CulturedDrosophila ProteinsFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeGene Expression Regulation, DevelopmentalMembrane PotentialsMushroom BodiesNeuronsCalciumCalcium-Binding ProteinsDrosophila ProteinsFMR1 protein, DrosophilaFragile X Messenger Ribonucleoprotein 1

Identifiers

PMID20843478
PMCPMC2982942
OpenAlexW2094800813

What OpenQuestion holds

Textmetadata
LicenceTDM
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.