Evidence map›Paper›PMID 26937011›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016

Essential Roles for ARID1B in Dendritic Arborization and Spine Morphology of Developing Pyramidal Neurons.

Minhan Ka, Divyan A Chopra, Shashank M Dravid, Woo-Yang Kim

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.5field-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

55 citing papers in PubMed, 80 citations in OpenAlex.

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  19. Case report: A novelFrontiers in psychiatry · 2024
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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

4 authors at 2 institutions in 1 country.

Minhan KaDepartment of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska 68198, and.
Divyan A ChopraDepartment of Pharmacology, Creighton University, Omaha, Nebraska 68178.
Shashank M DravidDepartment of Pharmacology, Creighton University, Omaha, Nebraska 68178.
Woo-Yang KimDepartment of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska 68198, and wooyang.kim@unmc.edu.
Creighton University · USNebraska Medical Center · US

Funding

UNMC Histology/Imaging and Creighton University Imaging Core FacilityP30GM110768 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SMITH, SHELLEY D · 2014 to 2018
$5.1M
The Molecular Biology of Neurosurgery SystemsP20GM103471 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SMITH, SHELLEY D · 2012 to 2013
$4.1M
Functional Characterization of a Causative Gene for Intellectual DisabilityR01NS091220 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI KIM, WOO-YANG · 2015 to 2019
$1.7M
NIGMS NIH HHS P20 GM103471NIGMS NIH HHS P20-GM-103471NIGMS NIH HHS P30 GM110768NINDS NIH HHS R01 NS091220NINDS NIH HHS R01-NS-091220
6 · The paper itself

Abstract

De novo truncating mutations in ARID1B, a chromatin-remodeling gene, cause Coffin-Siris syndrome, a developmental disorder characterized by intellectual disability and speech impairment; however, how the genetic elimination leads to cognitive dysfunction remains unknown. Thus, we investigated the neural functions of ARID1B during brain development. Here, we show that ARID1B regulates dendritic differentiation in the developing mouse brain. We knocked down ARID1B expression in mouse pyramidal neurons using in utero gene delivery methodologies. ARID1B knockdown suppressed dendritic arborization of cortical and hippocampal pyramidal neurons in mice. The abnormal development of dendrites accompanied a decrease in dendritic outgrowth into layer I. Furthermore, knockdown of ARID1B resulted in aberrant dendritic spines and synaptic transmission. Finally, ARID1B deficiency led to altered expression of c-Fos and Arc, and overexpression of these factors rescued abnormal differentiation induced by ARID1B knockdown. Our results demonstrate a novel role for ARID1B in neuronal differentiation and provide new insights into the origin of cognitive dysfunction associated with developmental intellectual disability. SIGNIFICANCE STATEMENT: Haploinsufficiency of ARID1B, a component of chromatin remodeling complex, causes intellectual disability. However, the role of ARID1B in brain development is unknown. Here, we demonstrate that ARID1B is required for neuronal differentiation in the developing brain, such as in dendritic arborization and synapse formation. Our findings suggest that ARID1B plays a critical role in the establishment of cognitive circuitry by regulating dendritic complexity. Thus, ARID1B deficiency may cause intellectual disability via abnormal brain wiring induced by the defective differentiation of cortical neurons.

Indexed as

Dendritic SpinesAction PotentialsAnimalsAnimals, NewbornBrainCells, CulturedDNA-Binding ProteinsEmbryo, MammalianFemaleGene Expression Regulation, DevelopmentalGlial Fibrillary Acidic ProteinHumansMiceMicrotubule-Associated ProteinsNeuronal PlasticityNuclear ProteinsARID1B protein, humanDNA-Binding ProteinsGlial Fibrillary Acidic ProteinMicrotubule-Associated ProteinsNuclear ProteinsTranscription FactorsVesicular Glutamate Transport Protein 1Vesicular Inhibitory Amino Acid Transport ProteinsARID1Bchromatin remodeling complexdendrite arborizationintellectual disabilityspine

Identifiers

PMID26937011
PMCPMC4879215
OpenAlexW2292728605

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.