Evidence map›Paper›PMID 30287841›Full record

ArticleScientific reports2018

Genetic inhibition of an ATP synthase subunit extends lifespan in C. elegans.

Chen Xu, Wooseon Hwang, Dae-Eun Jeong, Youngjae Ryu, Chang Man Ha, Seung-Jae V Lee, Lulu Liu, Zhi Ming He

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 41 citations in OpenAlex.

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  15. Fisetin regulates gut microbiota to decrease CCR9American journal of translational research · 2020
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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

8 authors at 4 institutions in 2 countries.

Chen XuState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, 210023, China. xuchn@nju.edu.cn.
Wooseon HwangDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, 37673, South Korea.
Dae-Eun JeongDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, 37673, South Korea.
Youngjae RyuBrain Research Core Facilities, Korea Brain Research Institute, Daegu, 41068, South Korea.
Chang Man HaBrain Research Core Facilities, Korea Brain Research Institute, Daegu, 41068, South Korea.
Seung-Jae V LeeDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, 37673, South Korea.ORCID http://orcid.org/0000-0002-6103-156X
Lulu LiuState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Zhi Ming HeState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Pohang University of Science and Technology · KRKorea Brain Research Institute · KRNanjing University · CNChina Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mild inhibition of mitochondrial respiration leads to longevity. Disruption of mitochondrial respiratory components extends lifespan in Caenorhabditis elegans, but the effects appear to be complex and the underlying mechanism for lifespan regulation by mitochondrial respiratory genes is still not fully understood. Here, we investigated the role of Y82E9BR.3, a worm homolog of the ATP synthase subunit C, in modulating longevity in C. elegans. We found that the Y82E9BR.3 protein is localized in mitochondria and expressed in various tissues throughout development. RNAi knockdown of Y82E9BR.3 extends lifespan, decreases the accumulation of lipofuscin, and affects various physiological processes, including development delay, reproduction impairment and slow behavior. Further tissue-specific RNAi analysis showed that the intestine is a crucial organ for the longevity effects conferred by Y82E9BR.3 RNAi. Moreover, we demonstrated that lifespan extension by Y82E9BR.3 RNAi is associated with reduced mitochondrial function, as well as the suppression of complex I activity in mitochondria. Unexpectedly, Y82E9BR.3 RNAi knock down did not influence the whole-worm ATP level. Our findings first reveal the crucial role of Y82E9BR.3 in mitochondrial function and the underlying mechanism of how Y82E9BR.3 regulates lifespan in C. elegans.

Indexed as

AnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsCell RespirationIntestinesLipofuscinLongevityMitochondriaMitochondrial Proton-Translocating ATPasesPhenotypeProtein SubunitsRNA InterferenceCaenorhabditis elegans ProteinsLipofuscinMitochondrial Proton-Translocating ATPasesProtein SubunitsY82E9BR.3 protein, C elegans

Identifiers

PMID30287841
PMCPMC6172204
OpenAlexW2893295027

What OpenQuestion holds

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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 OpenQuestion graph.