Evidence map›Paper›PMID 27072046›Full record

ArticleAging cell2016

Age-associated de-repression of retrotransposons in the Drosophila fat body, its potential cause and consequence.

Haiyang Chen, Xiaobin Zheng, Danqing Xiao, Yixian Zheng

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
17.8field-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

68 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
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  14. Studying Cellular Senescence Using the Model Organism Drosophila melanogaster.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
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  19. Article
  20. Article

8 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Haiyang ChenKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, China.
Xiaobin ZhengDepartment of Embryology, Carnegie Institution for Science, Baltimore, MD, 21218, USA.
Danqing XiaoKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, China.
Yixian ZhengDepartment of Embryology, Carnegie Institution for Science, Baltimore, MD, 21218, USA.
Carnegie Institution for Science · USSun Yat-sen University · CN

Funding

Super-resolution microscopy of nuclear lamin and spindle envelope/matrix functionR01GM106023 · NIGMS · CARNEGIE INSTITUTION OF WASHINGTON, D.C. · PI GOLDMAN, ROBERT D, ZHENG, YIXIAN · 2013 to 2020
$3.5M
The function and assembly of the lamin-B spindle sheathR01GM056312 · NIGMS · CARNEGIE INSTITUTION OF WASHINGTON, D.C. · PI ZHENG, YIXIAN · 1997 to 2014
$2.7M
NIGMS NIH HHS R01 GM056312NIGMS NIH HHS R01 GM106023
6 · The paper itself

Abstract

Eukaryotic genomes contain transposable elements (TE) that can move into new locations upon activation. Since uncontrolled transposition of TEs, including the retrotransposons and DNA transposons, can lead to DNA breaks and genomic instability, multiple mechanisms, including heterochromatin-mediated repression, have evolved to repress TE activation. Studies in model organisms have shown that TEs become activated upon aging as a result of age-associated deregulation of heterochromatin. Considering that different organisms or cell types may undergo distinct heterochromatin changes upon aging, it is important to identify pathways that lead to TE activation in specific tissues and cell types. Through deep sequencing of isolated RNAs, we report an increased expression of many retrotransposons in the old Drosophila fat body, an organ equivalent to the mammalian liver and adipose tissue. This de-repression correlates with an increased number of DNA damage foci and decreased level of Drosophila lamin-B in the old fat body cells. Depletion of the Drosophila lamin-B in the young or larval fat body results in a reduction of heterochromatin and a corresponding increase in retrotransposon expression and DNA damage. Further manipulations of lamin-B and retrotransposon expression suggest a role of the nuclear lamina in maintaining the genome integrity of the Drosophila fat body by repressing retrotransposons.

Indexed as

AgingAnimalsDNA DamageDrosophila melanogasterDrosophila ProteinsFat BodyGene Expression Regulation, DevelopmentalHeterochromatinHistonesLaminsLysineMethylationModels, BiologicalRetroelementsDrosophila ProteinsHeterochromatinHistonesLaminsLam protein, DrosophilaLysineRetroelementsagingDNA damageheterochromatinLamin-Blamin Dm0retrotransposons

Identifiers

PMID27072046
PMCPMC4854910
OpenAlexW2341478154

What OpenQuestion 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 OpenQuestion graph.