Evidence map›Paper›PMID 32783930›Full record

ArticleCell reports2020

RAI1 Regulates Activity-Dependent Nascent Transcription and Synaptic Scaling.

Patricia M Garay, Alex Chen, Takao Tsukahara, Jean Carlos Rodríguez Díaz, Rafi Kohen, J Christian Althaus, Margarete A Wallner, Roman J Giger, Kevin S Jones, Michael A Sutton and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. bioRxiv : the preprint server for biology · 2026
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  16. Loss ofProceedings of the National Academy of Sciences of the United States of America · 2022
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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

11 authors at 1 institution in 1 country.

Patricia M GarayNeuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Alex ChenNeuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Takao TsukaharaDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA; Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI 48109, USA; Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA.
Jean Carlos Rodríguez DíazNeuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Rafi KohenNeuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
J Christian AlthausDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA; Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Margarete A WallnerCollege of Literature, Science, and the Arts, University of Michigan, Ann Arbor, MI 48109, USA.
Roman J GigerNeuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA; Cellular and Molecular Biology Graduate Program, University of Michigan Medical School, Ann Arbor, MI, 48109, USA; Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Kevin S JonesNeuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Department of Pharmacology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Michael A SuttonNeuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA; Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: masutton@umich.edu.
Shigeki IwaseNeuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: siwase@umich.edu.
University of Michigan · US

Funding

Development of the Basal Telencephalic Limbic SystemR01DA020140 · NIDA · GEORGETOWN UNIVERSITY · PI CORBIN, JOSHUA G · 2006 to 2020
$7.3M
Trans-synaptic control of presynaptic neurotransmitter releaseR01NS097498 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SUTTON, MICHAEL MARK ALEXANDER · 2016 to 2025
$3.8M
A Neuron-specific Methyl-histone Regulatory ComplexR01NS116008 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Shigeki Iwase · 2020 to 2026
$3.6M
Neutralizing epigenomes in neurodevelopment disordersR01NS089896 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI IWASE, SHIGEKI · 2015 to 2019
$2.1M
Exploring Neuron - Specific Histone Methylation DynamicsR21NS104774 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI IWASE, SHIGEKI · 2018 to 2019
$429k
NIDA NIH HHS R01 DA020140NINDS NIH HHS R01 NS089896NINDS NIH HHS R01 NS097498NINDS NIH HHS R01 NS116008NINDS NIH HHS R21 NS104774
6 · The paper itself

Abstract

Long-lasting forms of synaptic plasticity such as synaptic scaling are critically dependent on transcription. Activity-dependent transcriptional dynamics in neurons, however, remain incompletely characterized because most previous efforts relied on measurement of steady-state mRNAs. Here, we use nascent RNA sequencing to profile transcriptional dynamics of primary neuron cultures undergoing network activity shifts. We find pervasive transcriptional changes, in which ∼45% of expressed genes respond to network activity shifts. We further link retinoic acid-induced 1 (RAI1), the Smith-Magenis syndrome gene, to the transcriptional program driven by reduced network activity. Remarkable agreement among nascent transcriptomes, dynamic chromatin occupancy of RAI1, and electrophysiological properties of Rai1-deficient neurons demonstrates the essential roles of RAI1 in suppressing synaptic upscaling in the naive network, while promoting upscaling triggered by activity silencing. These results highlight the utility of bona fide transcription profiling to discover mechanisms of activity-dependent chromatin remodeling that underlie normal and pathological synaptic plasticity.

Indexed as

AnimalsCells, CulturedFemaleHumansMaleMiceNerve NetNeuronal PlasticityProsencephalonRatsRats, Sprague-DawleySynapsesTrans-ActivatorsTranscriptional ActivationTranscription FactorsRAI1 protein, humanRai1 protein, mouseTrans-ActivatorsTranscription Factorsactivity-dependent transcriptionBru-seqchromatin regulationnascent RNAneurodevelopmental disordersRAI1Smith-Magenis Syndromesynaptic scaling

Identifiers

PMID32783930
PMCPMC7418709
OpenAlexW3048598545

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.