Evidence map›Paper›PMID 35140229›Full record

ArticleNature communications2022

Histone H3K4me3 modification is a transgenerational epigenetic signal for lipid metabolism in Caenorhabditis elegans.

Qin-Li Wan, Xiao Meng, Chongyang Wang, Wenyu Dai, Zhenhuan Luo, Zhinan Yin, Zhenyu Ju, Xiaodie Fu, Jing Yang, Qunshan Ye and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.9field-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

52 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
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  15. Multimorbidity and animal models.Animal models and experimental medicine · 2025
    Review
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  19. Postbiotic pA1cInternational journal of molecular sciences · 2025
    Article
  20. Review
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

12 authors at 2 institutions in 1 country.

Qin-Li Wan *The Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.ORCID http://orcid.org/0000-0003-2864-912X
Xiao Meng *The Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.
Chongyang WangThe Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.ORCID http://orcid.org/0000-0003-2254-1871
Wenyu DaiThe Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.ORCID http://orcid.org/0000-0003-4669-5787
Zhenhuan LuoThe Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.ORCID http://orcid.org/0000-0003-1375-0882
Zhinan YinThe Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.ORCID http://orcid.org/0000-0001-6524-8777
Zhenyu JuKey Laboratory of Regenerative Medicine of Ministry of Education, Institute of Aging and Regeneration Medicine, Jinan University, Guangzhou, Guangdong, 510632, China.ORCID http://orcid.org/0000-0002-9525-6521
Xiaodie FuThe Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.
Jing YangThe Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.ORCID http://orcid.org/0000-0002-9498-608X
Qunshan YeThe Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China.ORCID http://orcid.org/0000-0003-1785-2931
Zhan-Hui ZhangThe First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510632, China.
Qinghua ZhouThe Sixth Affiliated Hospital of Jinan University, Jinan University, Dongguan, 523560, Guangdong, China. gene@email.jnu.edu.cn.ORCID http://orcid.org/0000-0003-0468-9266
Jinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

As a major risk factor to human health, obesity presents a massive burden to people and society. Interestingly, the obese status of parents can cause progeny's lipid accumulation through epigenetic inheritance in multiple species. To date, many questions remain as to how lipid accumulation leads to signals that are transmitted across generations. In this study, we establish a nematode model of C. elegans raised on a high-fat diet (HFD) that leads to measurable lipid accumulation, which can transmit the lipid accumulation signal to their multigenerational progeny. Using this model, we find that transcription factors DAF-16/FOXO and SBP-1/SREBP, nuclear receptors NHR-49 and NHR-80, and delta-9 desaturases (fat-5, fat-6, and fat-7) are required for transgenerational lipid accumulation. Additionally, histone H3K4 trimethylation (H3K4me3) marks lipid metabolism genes and increases their transcription response to multigenerational obesogenic effects. In summary, this study establishes an interaction between a network of lipid metabolic genes and chromatin modifications, which work together to achieve transgenerational epigenetic inheritance of obesogenic effects.

Indexed as

Epigenesis, GeneticLipid MetabolismAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDiet, High-FatEpigenomicsHeredityHistonesHumansInheritance PatternsProtein Processing, Post-TranslationalReceptors, Cytoplasmic and NuclearCaenorhabditis elegans Proteinshistone H3 trimethyl Lys4HistonesReceptors, Cytoplasmic and Nuclear

Identifiers

PMID35140229
PMCPMC8828817
OpenAlexW4220974069

What Socratic holds

Textmetadata
LicenceCC BY
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.