Evidence map›Paper›PMID 39707500›Full record

ArticleCell & bioscience2024

Impact of c-JUN deficiency on thalamus development in mice and human neural models.

Jiantao Shi, Qing Chen, Jianheng Lai, Jieying Zhu, Ran Zhang, Md Abdul Mazid, Dongwei Li, Huanxing Su, Dajiang Qin

Abstract read
In one paragraph

Article in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

1 citing paper in PubMed.

  1. 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

9 authors.

Jiantao ShiState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
Qing ChenKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jianheng LaiGuangdong Engineering Technology Research Center of Biological Targeting Diagnosis, Therapy and Rehabilitation, The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Jieying ZhuCAS Key Laboratory of Regenerative Biology, Center for Cell Lineage and Development, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Ran ZhangState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
Md Abdul MazidLaboratory of Integrative Biology, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Dongwei LiKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. lidongwei@gzhmu.edu.cn.
Huanxing SuState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China. huanxingsu@um.edu.mo.ORCID http://orcid.org/0000-0003-3254-825X
Dajiang QinKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. qin_dajiang@gzhmu.edu.cn.

Funding

Guangzhou Core Medical Disciplines Project (2021-2023) Guangzhou Core Medical Disciplines Project (2021-2023)Key Laboratory of Guangdong Higher Education Institutes 2021KSYS009Macau Science and Technology Development Fund 0061/2021/A2Research Funds from Health @ InnoHK Programlaunched by Innovation Technology Commission of the Hong Kong SAR, P. R. China Research Funds from Health @ InnoHK Programlaunched by Innovation Technology Commission of the Hong Kong SAR, P. R. ChinaShenzhen Science and Technology Innovation Commission EF026/ICMS-SHX/2022/SZSTIC
6 · The paper itself

Abstract

backgroundc-Jun is a key regulator of gene expression. Through the formation of homo- or heterodimers, c-JUN binds to DNA and regulates gene transcription. While c-Jun plays a crucial role in embryonic development, its impact on nervous system development in higher mammals, especially for some deep structures, for example, thalamus in diencephalon, remains unclear.

methodsTo investigate the influence of c-JUN on early nervous system development, c-Jun knockout (KO) mice and c-JUN KO H1 embryonic stem cells (ESCs)-derived neural progenitor cells (NPCs), cerebral organoids (COs), and thalamus organoids (ThOs) models were used. We detected the dysplasia via histological examination and immunofluorescence staining, omics analysis, and loss/gain of function analysis.

resultsAt embryonic day 14.5, c-Jun knockout (KO) mice exhibited sparseness of fibers in the brain ventricular parenchyma and malformation of the thalamus in the diencephalon. The absence of c-JUN accelerated the induction of NPCs but impaired the extension of fibers in human neuronal cultures. COs lacking c-JUN displayed a robust PAX6

conclusionOur findings from in vivo and in vitro experiments indicate that c-JUN depletion impedes the extension of nerve fibers and renders the thalamus susceptible to dysplasia during early mouse embryonic development and human ThO patterning. Our work provides evidence for the first time that c-JUN is a key transcription regulator that play important roles in the thalamus/diencephalon development.

Indexed as

AP-1Cerebral organoidsc-JUNNeural developmentNPCThalamus organoids

Identifiers

PMID39707500
PMCPMC11662577

What Socratic holds

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Registered trials

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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 Socratic graph.