Evidence map›Paper›PMID 34145365›Full record

ArticleCommunications biology2021

Loss of histone methyltransferase ASH1L in the developing mouse brain causes autistic-like behaviors.

Yuen Gao, Natalia Duque-Wilckens, Mohammad B Aljazi, Yan Wu, Adam J Moeser, George I Mias, Alfred J Robison, Jin He

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Novel heterozygousFrontiers in neurology · 2025
    Article
  5. Chromatin modifiers in neurodevelopment.Frontiers in molecular neuroscience · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. ASH1L contributes to oocyte apoptosis by regulating DNA damage.American journal of physiology. Cell physiology · 2022
    Article
  13. Article
  14. Frontiers in behavioral neuroscience · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

8 authors at 2 institutions in 1 country.

Yuen Gao *Department of Biochemistry and Molecular Biology, College of Natural Science, Michigan State University, East Lansing, MI, USA.ORCID 0000-0002-2807-2976
Natalia Duque-Wilckens *Department of Physiology, College of Natural Science, Michigan State University, East Lansing, MI, USA.
Mohammad B AljaziDepartment of Biochemistry and Molecular Biology, College of Natural Science, Michigan State University, East Lansing, MI, USA.
Yan WuDepartment of Biochemistry and Molecular Biology, College of Natural Science, Michigan State University, East Lansing, MI, USA.
Adam J MoeserDepartment of Physiology, College of Natural Science, Michigan State University, East Lansing, MI, USA.ORCID 0000-0003-3068-627X
George I MiasDepartment of Biochemistry and Molecular Biology, College of Natural Science, Michigan State University, East Lansing, MI, USA.ORCID 0000-0002-9083-1216
Alfred J RobisonDepartment of Physiology, College of Natural Science, Michigan State University, East Lansing, MI, USA.
Jin HeDepartment of Biochemistry and Molecular Biology, College of Natural Science, Michigan State University, East Lansing, MI, USA. hejin1@msu.edu.ORCID 0000-0001-8283-7952
Michigan State University · USMichigan Department of Agriculture and Rural Development · US

Funding

Projection-specific gene expression in resilience to chronic stressR01MH111604 · NIMH · MICHIGAN STATE UNIVERSITY · PI Michelle Suzanne Mazei-Robison, ALFRED J ROBISON · 2016 to 2026
$4.9M
Neuro-Immune Mechanisms in Early Life Stress-Induced Gastrointestinal DiseaseR01HD072968 · NICHD · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI MOESER, ADAM, ROBISON, ALFRED J · 2013 to 2023
$3.8M
Epigenetic mechanisms of Ash1L in transcriptional activationR01GM127431 · NIGMS · MICHIGAN STATE UNIVERSITY · PI HE, JIN · 2018 to 2022
$1.7M
NICHD NIH HHS R01 HD072968NIGMS NIH HHS R01 GM127431NIMH NIH HHS R01 MH111604
6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disease associated with various gene mutations. Recent genetic and clinical studies report that mutations of the epigenetic gene ASH1L are highly associated with human ASD and intellectual disability (ID). However, the causality and underlying molecular mechanisms linking ASH1L mutations to genesis of ASD/ID remain undetermined. Here we show loss of ASH1L in the developing mouse brain is sufficient to cause multiple developmental defects, core autistic-like behaviors, and impaired cognitive memory. Gene expression analyses uncover critical roles of ASH1L in regulating gene expression during neural cell development. Thus, our study establishes an ASD/ID mouse model revealing the critical function of an epigenetic factor ASH1L in normal brain development, a causality between Ash1L mutations and ASD/ID-like behaviors in mice, and potential molecular mechanisms linking Ash1L mutations to brain functional abnormalities.

Indexed as

AnimalsAutism Spectrum DisorderBrainDisease Models, AnimalDNA-Binding ProteinsEmbryonic DevelopmentHistone-Lysine N-MethyltransferaseHumansIntellectual DisabilityMiceMice, Inbred C57BLMice, KnockoutAsh1l protein, mouseDNA-Binding ProteinsHistone-Lysine N-Methyltransferase

Identifiers

PMID34145365
PMCPMC8213741
OpenAlexW3172996380

What OpenQuestion holds

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LicenceCC BY
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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.