Evidence map›Paper›PMID 39455502›Full record

ArticleScience China. Life sciences2025

SETD3-mediated histidine methylation of MCM7 regulates DNA replication by facilitating chromatin loading of MCM.

Hongguo Duan, Shuang Wang, Wen-Jie Shu, Yongjia Tong, Hai-Zhen Long, Guohong Li, Hai-Ning Du, Meng-Jie Zhao

Abstract read
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In one paragraph

Article in Science China. Life sciences, 2025. 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

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

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

8 authors.

Hongguo Duan *Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Frontier Science Center for Immunology and Metabolism, Emergency Center, Zhongnan Hospital of Wuhan University, RNA Institute, Wuhan University, Wuhan, 430072, China.
Shuang Wang *Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Frontier Science Center for Immunology and Metabolism, Emergency Center, Zhongnan Hospital of Wuhan University, RNA Institute, Wuhan University, Wuhan, 430072, China.
Wen-Jie ShuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Frontier Science Center for Immunology and Metabolism, Emergency Center, Zhongnan Hospital of Wuhan University, RNA Institute, Wuhan University, Wuhan, 430072, China.
Yongjia TongThe Institute for Advanced Studies, Wuhan University, Wuhan, 430072, China.
Hai-Zhen LongShenzhen Bay Laboratory, Shenzhen, 518083, China.
Guohong LiHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, 430072, China.
Hai-Ning DuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Frontier Science Center for Immunology and Metabolism, Emergency Center, Zhongnan Hospital of Wuhan University, RNA Institute, Wuhan University, Wuhan, 430072, China. hainingdu@whu.edu.cn.
Meng-Jie ZhaoHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Frontier Science Center for Immunology and Metabolism, Emergency Center, Zhongnan Hospital of Wuhan University, RNA Institute, Wuhan University, Wuhan, 430072, China. mjzhao@whu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The minichromosome maintenance complex (MCM) DNA helicase is an important replicative factor during DNA replication. The proper chromatin loading of MCM is a key step to ensure replication initiation during S phase. Because replication initiation is regulated by multiple biological cues, additional changes to MCM may provide better understanding towards this event. Here, we report that histidine methyltransferase SETD3 promotes DNA replication in a manner dependent on enzymatic activity. Nascent-strand sequencing (NS-seq) shows that SETD3 regulates replication initiation, as depletion of SETD3 attenuates early replication origins firing. Biochemical studies reveal that SETD3 binds MCM mainly during S phase, which is required for the CDT1-mediated chromatin loading of MCM. This MCM loading relies on histidine-459 methylation (H459me) on MCM7 which is catalyzed by SETD3. Impairment of H459 methylation attenuates DNA synthesis and chromatin loading of MCM. Furthermore, we show that CDK2 phosphorylates SETD3 at Serine-21 during the G1/S phase, which is required for DNA replication and cell cycle progression. These findings demonstrate a novel mechanism by which SETD3 methylates MCM to regulate replication initiation.

Indexed as

ChromatinDNA ReplicationHistidineMethyltransferasesMinichromosome Maintenance Complex Component 7HeLa CellsHistone MethyltransferasesHumansMethylationPhosphorylationS PhaseChromatinHistidineHistone MethyltransferasesMCM7 protein, humanMethyltransferasesMinichromosome Maintenance Complex Component 7SETD3 protein, humanDNA replicationhistidine methylationMCMreplication origin firingSETD3

Identifiers

PMID39455502

What OpenQuestion 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 OpenQuestion graph.