Evidence map›Paper›PMID 41379335›Full record

ArticleCellular and molecular life sciences : CMLS2025

The methyltransferase N6amt1 regulates hippocampal neurogenesis through 6 mA modification of Txnrd3 DNA.

Yuanfei Wu, Wenhui Ma, Qingqing Li, Yang Li, Linjie Xie, Xuejian Kong, Shuwei Chen, Qian Wang, Aiguo Xuan

Abstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 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

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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

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

9 authors.

Yuanfei Wu *Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Wenhui Ma *Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Qingqing Li *Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Yang LiInstitute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Linjie XieInstitute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xuejian KongThe Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, China.
Shuwei ChenInstitute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Qian WangInstitute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Aiguo XuanInstitute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, School of Basic Medical Sciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. xag2005@163.com.ORCID http://orcid.org/0000-0002-8574-576X

Funding

National Natural Science Foundation of China 81371217Natural Science Foundation of Guangdong Province 2022A1515012121, 2023A1515010292the open research funds from the Sixth Affiliated Hospital of Guangzhou Medical University 202201-207
6 · The paper itself

Abstract

N6-methyladenine (6 mA), the most prevalent DNA modification in mammals and other eukaryotes, regulates DNA mismatch repair, chromosome replication, and transcription. However, its role in adult hippocampal neurogenesis remains unkown. Here we showed that the methyltransferase N6amt1 and 6 mA modification were highly enriched in hippocampal neurons both in vitro and in vivo. Functionally, knockdown of N6amt1 in neural stem cells (NSCs) significantly reduced 6 mA levels, neuronal genesis, and proliferation while promoting glial differentiation. Conversely, N6amt1 overexpression enhanced neuronal differentiation and proliferation. Mechanistically, N6amt1-mediated 6 mA modification of Txnrd3 DNA increased its transcription, thereby promoting hippocampal neurogenesis. Furthermore, exogenous Txnrd3 overexpression rescued the defects in cell differentiation and proliferation induced by N6amt1 depletion. Notably, N6amt1 deficiency impaired hippocampal neurogenesis and spatial memory in adult mice. Our findings highlight the critical role of DNA 6 mA in N6amt1-mediated neurogenesis and suggest that targeting N6amt1 may offer a novel therapeutic strategy for neurological disorders associated with cognitive impairment.

Indexed as

AdenineHippocampusMethyltransferasesNeurogenesisAnimalsCell DifferentiationCell ProliferationCells, CulturedHumansMaleMiceMice, Inbred C57BLNeural Stem CellsNeuronsAdenineMethyltransferasesLearning and memoryN6amt1N6-methyladenineNeurogenesisTxnrd3

Identifiers

PMID41379335
PMCPMC12775215

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.