Evidence map›Paper›PMID 41888895›Full record

ArticleCell & bioscience2026

Spontaneous whole genome duplication renders mouse embryonic fibroblasts resistant to reprogramming.

Wei Li, Lingyu Zhong, Pengli Li, Ziwei Zhai, Runxia Lin, Minjing Ke, Yixin Fan, Yu Liu, Yu Fu, Yue Qin and 4 more

Abstract read
In one paragraph

Article in Cell & bioscience, 2026. 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

14 authors.

Wei LiGuangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China.
Lingyu ZhongLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Pengli LiLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Ziwei ZhaiLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Runxia LinLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Minjing KeGuangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China.
Yixin FanGuangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China.
Yu LiuLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Yu FuLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Yue QinLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Chengchen ZhaoLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Bo WangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Junqi KuangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China. kuangjunqi@westlake.edu.cn.
Duanqing PeiLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China. peiduanqing@westlake.edu.cn.

Funding

Key R&D Program of Zhejiang 2024SSYS0033National Natural Science Foundation of China 32300639National Natural Science Foundation of China 92068201
6 · The paper itself

Abstract

Whole-genome duplication (WGD) is thought to be quite rare, but has important implications ranging from emergences of new species to tumorigenesis. The burden of doubled genome for a cell must be traumatic and remains poorly understood. Here we report a spontaneous and robust WGD system amicable to detailed molecular analysis. We first show that mouse embryonic fibroblasts (MEFs) undergo spontaneous WGD in vitro. The resulting binucleated cells or BNCs become resistant to iPSC reprogramming. We further show that pretreating MEFs with p38 inhibitor SB203580 suppresses WGD and enhances reprogramming. Mechanistically, we demonstrate the WGD activates p53 in BNCs to act as the primary barrier to reprogramming, as its depletion rescues iPSC formation in tetraploid cells. These findings provide a convenient WGD experimental system and our preliminary analysis reveals p38 coordinates WGD progression and p53 regulates subsequent cell fate determination in genome-doubled cells.

Indexed as

Cell fate controlCell fate transitionp38p53Somatic cell reprogrammingTetraploid cellsWhole-genome duplication (WGD)

Identifiers

PMID41888895
PMCPMC13147676

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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.