Evidence map›Paper›PMID 37130870›Full record

ArticleCell discovery2023

Critically short telomeres derepress retrotransposons to promote genome instability in embryonic stem cells.

Nannan Zhao, Guoxing Yin, Chun Liu, Weiyu Zhang, Yang Shen, Dan Wang, Zhenzhen Lin, Jiao Yang, Jian Mao, Renpeng Guo and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
19.9field-weighted citation impact, top 1% of its field
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

10 citing papers in PubMed, 46 citations in OpenAlex.

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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

15 authors at 4 institutions in 2 countries.

Nannan Zhao *State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Guoxing Yin *State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Chun Liu *State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Weiyu ZhangState Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Yang ShenGenome Institute of Singapore, Singapore, Singapore.
Dan Wang2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Department of Immunology, Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Zhenzhen Lin2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Department of Immunology, Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Jiao YangState Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Jian MaoState Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Renpeng GuoState Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Yongwang ZhangState Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Feng WangDepartment of Genetics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Zhe Liu2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Department of Immunology, Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China. zheliu@tmu.edu.cn.ORCID http://orcid.org/0000-0002-2536-4180
Xinyi LuState Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China. luxy@nankai.edu.cn.ORCID http://orcid.org/0000-0002-3885-3960
Lin LiuState Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China. liulin@nankai.edu.cn.ORCID http://orcid.org/0000-0001-9881-6830
Nankai University · CNTianjin Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNGenome Institute of Singapore · SG

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32030033National Natural Science Foundation of China (National Science Foundation of China) 32070858
6 · The paper itself

Abstract

Telomeres, at the ends of chromosomes, protect chromosomes from fusion and preserve genomic stability. However, the molecular mechanisms underlying telomere attrition-induced genome instability remain to be understood. We systematically analyzed the expression of retrotransposons and performed genomic sequencing of different cell and tissue types with telomeres of varying lengths due to telomerase deficiency. We found that critically short telomeres altered retrotransposon activity to promote genomic instability in mouse embryonic stem cells, as evidenced by elevated numbers of single nucleotide variants, indels and copy number variations (CNVs). Transpositions of retrotransposons such as LINE1 resulting from the short telomeres can also be found in these genomes with elevated number of mutations and CNVs. Retrotransposon activation is linked to increased chromatin accessibility, and reduced heterochromatin abundance correlates with short telomeres. Re-elongation of telomeres upon recovery of telomerase partly represses retrotransposons and heterochromatin accumulation. Together, our findings suggest a potential mechanism by which telomeres maintain genomic stability by suppressing chromatin accessibility and retrotransposon activity.

Identifiers

PMID37130870
PMCPMC10154409
OpenAlexW4367834414

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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.