Evidence map›Paper›PMID 41423560›Full record

ArticleNature communications2025

Chromatin remodeling factor BAF155 coordinates oligodendroglial-neuronal communications linked to regional myelination and autism-like behavioral deficits in mice.

Xiaorui Wang, Cong Zeng, Zhonghao Wu, Minmin Lu, Xiao Wang, Yun Xiu, Qi Wang, Shouyu Wang, Xiaoying Chen, Yan Shen and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

21 authors.

Xiaorui WangDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
Cong ZengBiomedical Analysis Research Centre, Third Military Medical University, Chongqing, China.ORCID http://orcid.org/0009-0009-9212-920X
Zhonghao WuDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
Minmin LuDepartment of Physiology, Institute of Brain and Intelligence, Third Military Medical University, Chongqing, China.
Xiao WangDepartment of Physiology, Institute of Brain and Intelligence, Third Military Medical University, Chongqing, China.
Yun XiuDepartment of Neurobiology, School of Basic Medical Sciences; Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), Chongqing Medical University, Chongqing, China.
Qi WangDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
Shouyu WangDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
Xiaoying ChenDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
Yan ShenDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
Hui LiDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
Yixun SuDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China.
Penghui ChenDepartment of Neurobiology, Third Military Medical University, Chongqing, China.
Hui ChenSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, NSW, Australia.ORCID http://orcid.org/0000-0001-6883-3752
Nengyin ShengState Key Laboratory of Genetic Resources and Evolution, Key Laboratory of Animal Models and Human Disease Mechanisms of Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China.ORCID http://orcid.org/0000-0003-3086-3950
Wei MoSir Run Run Shaw Hospital, Department of Immunology, School of Basic Medical Science, Zhejiang University, Hangzhou, China.ORCID http://orcid.org/0000-0002-8165-4473
Chenju YiSeventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.ORCID http://orcid.org/0000-0002-8686-4525
Qingwu YangDepartment of Neurology, Second Affiliated Hospital, Chongqing Institute for Brain and Intelligence, Third Military Medical University, Chongqing, China.
Alexei VerkhratskyFaculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.ORCID http://orcid.org/0000-0003-2592-9898
Jianqin NiuDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China. jianqinniu@tmmu.edu.cn.ORCID http://orcid.org/0000-0003-0642-7542
Lan XiaoDepartment of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China. xiaolan35@hotmail.com.ORCID http://orcid.org/0000-0002-0391-6909

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32271034National Natural Science Foundation of China (National Science Foundation of China) W2511095
6 · The paper itself

Abstract

Autism spectrum disorders (ASD) are neurodevelopmental disorders associated with synaptic deficits. Oligodendrocyte precursor cells (OPCs) are the only type of glial cells that establish direct synaptic connections with neurons within the central nervous system (CNS). However, the mechanism that results in the delicate construction of OPC-neuron synaptic connections remain poorly understood. Here we show in a mouse model that BAF155, a chromatin remodeling factor, is highly expressed in committed OPCs. BAF155 influences the OPC differentiation and myelination by coordinating the expression of multiple synapse-related genes that mediate OPC-neuron synaptic communication. The varying chromatin regulatory roles of BAF155 across brain regions give rise to local myelin deficits, contributing to the diverse clinical manifestations observed in individuals with ASD. Collectively, these results deepen our insight into OPC-neuron interactions under pathophysiological conditions and uncover a mechanism that integrates synaptic and ASD susceptibility genes, implying that abnormal OPC-neuron synaptogenesis could be an early instigator of ASD.

Indexed as

Autism Spectrum DisorderAutistic DisorderMyelin SheathNeuronsOligodendrogliaTranscription FactorsAnimalsBehavior, AnimalBrainCell CommunicationCell DifferentiationChromatin Assembly and DisassemblyDisease Models, AnimalFemaleHumansMaleTranscription Factors

Identifiers

PMID41423560
PMCPMC12859018

What OpenQuestion holds

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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.