Evidence map›Paper›PMID 29898393›Full record

ArticleCell reports2018

Activity-Induced Regulation of Synaptic Strength through the Chromatin Reader L3mbtl1.

Wenjie Mao, Anna C Salzberg, Motokazu Uchigashima, Yuto Hasegawa, Hanno Hock, Masahiko Watanabe, Schahram Akbarian, Yuka Imamura Kawasawa, Kensuke Futai

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Diverging from the Norm: Reevaluating What Miniature Excitatory Postsynaptic Currents Tell Us about Homeostatic Synaptic Plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Contribution of NAADP to Glutamate-Evoked Changes in CaFrontiers in cell and developmental biology · 2020
    Article
  16. Firing Rate Homeostasis Can Occur in the Absence of Neuronal Activity-Regulated Transcription.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  17. The neuronal stimulation-transcription coupling map.Current opinion in neurobiology · 2019
    Review
  18. The chromatin landscape of neuronal plasticity.Current opinion in neurobiology · 2019
    Review
  19. Review
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

9 authors at 6 institutions in 2 countries.

Wenjie MaoBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605-2324, USA.
Anna C SalzbergDepartment of Pharmacology, Department of Biochemistry and Molecular Biology, and Institute for Personalized Medicine, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033, USA.
Motokazu UchigashimaBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605-2324, USA; Department of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan.
Yuto HasegawaBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605-2324, USA.
Hanno HockCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Harvard Medical School,185 Cambridge Street, Boston, MA 02114, USA.
Masahiko WatanabeDepartment of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan.
Schahram AkbarianMount Sinai Department of Psychiatry, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029, USA.
Yuka Imamura KawasawaDepartment of Pharmacology, Department of Biochemistry and Molecular Biology, and Institute for Personalized Medicine, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033, USA.
Kensuke FutaiBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605-2324, USA. Electronic address: kensuke.futai@umassmed.edu.
Neuropsychiatric Research Institute · USPennsylvania State University · USHokkaido University · JPIcahn School of Medicine at Mount Sinai · USMassachusetts General Hospital · USUniversity of Massachusetts Chan Medical School · US

Funding

REPRESSIVE HISTONE AND DNA METHYLATION IN RODENT DEPRESSION MODELSP50MH096890 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ALLIS, CHARLES DAVID · 2012 to 2021
$20.2M
Neurodevelopmental Phenotypes in MLL mutant miceR01MH104341 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI AKBARIAN, SCHAHRAM · 2015 to 2019
$2.1M
Functional analysis of Neuroligin-Neurexin interactions in synaptic transmissionR01NS085215 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FUTAI, KENSUKE · 2014 to 2018
$1.8M
NIMH NIH HHS P50 MH096890NIMH NIH HHS R01 MH104341NINDS NIH HHS R01 NS085215
6 · The paper itself

Abstract

Homeostatic synaptic downscaling reduces neuronal excitability by modulating the number of postsynaptic receptors. Histone modifications and the subsequent chromatin remodeling play critical roles in activity-dependent gene expression. Histone modification codes are recognized by chromatin readers that affect gene expression by altering chromatin structure. We show that L3mbtl1 (lethal 3 malignant brain tumor-like 1), a polycomb chromatin reader, is downregulated by neuronal activity and is essential for synaptic response and downscaling. Genome-scale mapping of L3mbtl1 occupancies identified Ctnnb1 as a key gene downstream of L3mbtl1. Importantly, the occupancy of L3mbtl1 on the Ctnnb1 gene was regulated by neuronal activity. L3mbtl1 knockout neurons exhibited reduced Ctnnb1 expression. Partial knockdown of Ctnnb1 in wild-type neurons reduced excitatory synaptic transmission and abolished homeostatic downscaling, and transfecting Ctnnb1 in L3mbtl1 knockout neurons enhanced synaptic transmission and restored homeostatic downscaling. These results highlight a role for L3mbtl1 in regulating homeostasis of synaptic efficacy.

Indexed as

Animalsbeta CateninCells, CulturedChromatinHippocampusHistonesMiceMice, Inbred C57BLMice, KnockoutNuclear ProteinsPicrotoxinPromoter Regions, GeneticRepressor ProteinsRNA InterferenceRNA, Small InterferingSynaptic Transmissionbeta CateninChromatinCTNNB1 protein, mouseHistonesL3MBTL1 protein, mouseNuclear ProteinsPicrotoxinRepressor ProteinsRNA, Small InterferingTumor Suppressor Proteinschromatin readerglutamate receptorhippocampushomeostatic plasticityneuronal activitysynaptic scalingsynaptic transmission

Identifiers

PMID29898393
PMCPMC6309677
OpenAlexW2807755028

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.