Evidence map›Paper›PMID 29472612›Full record

ArticleNature communications2018

Sumoylation regulates FMRP-mediated dendritic spine elimination and maturation.

Anouar Khayachi, Carole Gwizdek, Gwénola Poupon, Damien Alcor, Magda Chafai, Frédéric Cassé, Thomas Maurin, Marta Prieto, Alessandra Folci, Fabienne De Graeve and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
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  5. Cells · 2024
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  15. FMRP Sustains Presynaptic Function via Control of Activity-Dependent Bulk Endocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    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

20 authors at 2 institutions in 1 country.

Anouar KhayachiUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Carole GwizdekUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Gwénola PouponUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Damien AlcorUniversité Côte d'Azur, INSERM, C3M, 06200, Nice, France.
Magda ChafaiUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Frédéric CasséUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Thomas MaurinUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Marta PrietoUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Alessandra FolciUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Fabienne De GraeveUniversité Côte d'Azur, CNRS, INSERM, iBV, 06108, Nice, France.
Sara CastagnolaUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Romain GautierUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Lenka SchorovaUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Céline LoriolUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Marie PronotUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Florence BesseUniversité Côte d'Azur, CNRS, INSERM, iBV, 06108, Nice, France.
Frédéric BrauUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Emmanuel DevalUniversité Côte d'Azur, CNRS, IPMC, 06560, Valbonne, France.
Barbara BardoniUniversité Côte d'Azur, INSERM, CNRS, IPMC, 06560, Valbonne, France.ORCID http://orcid.org/0000-0001-6411-1517
Stéphane MartinUniversité Côte d'Azur, INSERM, CNRS, IPMC, 06560, Valbonne, France. martin@ipmc.cnrs.fr.ORCID http://orcid.org/0000-0001-6771-7645
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fragile X syndrome (FXS) is the most frequent inherited cause of intellectual disability and the best-studied monogenic cause of autism. FXS results from the functional absence of the fragile X mental retardation protein (FMRP) leading to abnormal pruning and consequently to synaptic communication defects. Here we show that FMRP is a substrate of the small ubiquitin-like modifier (SUMO) pathway in the brain and identify its active SUMO sites. We unravel the functional consequences of FMRP sumoylation in neurons by combining molecular replacement strategy, biochemical reconstitution assays with advanced live-cell imaging. We first demonstrate that FMRP sumoylation is promoted by activation of metabotropic glutamate receptors. We then show that this increase in sumoylation controls the homomerization of FMRP within dendritic mRNA granules which, in turn, regulates spine elimination and maturation. Altogether, our findings reveal the sumoylation of FMRP as a critical activity-dependent regulatory mechanism of FMRP-mediated neuronal function.

Indexed as

SumoylationAmino Acid SequenceAnimalsCells, CulturedDendritic SpinesFemaleFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeHumansMaleMiceMice, Inbred C57BLMice, KnockoutModels, MolecularModels, NeurologicalPhenotypeFragile X Messenger Ribonucleoprotein 1Recombinant ProteinsRNA, Messenger

Identifiers

PMID29472612
PMCPMC5823917
OpenAlexW2793138755

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.