Evidence map›Paper›PMID 27001890›Full record

ArticleNature communications2016

Mondo complexes regulate TFEB via TOR inhibition to promote longevity in response to gonadal signals.

Shuhei Nakamura, Özlem Karalay, Philipp S Jäger, Makoto Horikawa, Corinna Klein, Kayo Nakamura, Christian Latza, Sven E Templer, Christoph Dieterich, Adam Antebi

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

64 citing papers in PubMed, 98 citations in OpenAlex.

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  11. MondoA and AKI and AKI-to-CKD Transition.Journal of the American Society of Nephrology : JASN · 2024
    Article
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  13. Review
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  15. Article
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  17. Article
  18. Neuronal MML-1/MXL-2 regulates systemic aging via glutamate transporter and cell nonautonomous autophagic and peroxidase activity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. Article

4 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

10 authors at 5 institutions in 3 countries.

Shuhei NakamuraDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, Cologne 50931, Germany.
Özlem KaralayDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, Cologne 50931, Germany.
Philipp S JägerDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, Cologne 50931, Germany.
Makoto HorikawaDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, Cologne 50931, Germany.
Corinna KleinDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, Cologne 50931, Germany.
Kayo NakamuraDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, Cologne 50931, Germany.
Christian LatzaDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, Cologne 50931, Germany.
Sven E TemplerComputational RNA Biology and Ageing, Max Planck Institute for Biology of Ageing, Cologne 50931, Germany.
Christoph DieterichComputational RNA Biology and Ageing, Max Planck Institute for Biology of Ageing, Cologne 50931, Germany.
Adam AntebiDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Joseph Stelzmann Strasse 9b, Cologne 50931, Germany.
Max Planck Institute for Biology of Ageing · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEHamamatsu University School of Medicine · JPKlaus Tschira Foundation · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Germline removal provokes longevity in several species and shifts resources towards survival and repair. Several Caenorhabditis elegans transcription factors regulate longevity arising from germline removal; yet, how they work together is unknown. Here we identify a Myc-like HLH transcription factor network comprised of Mondo/Max-like complex (MML-1/MXL-2) to be required for longevity induced by germline removal, as well as by reduced TOR, insulin/IGF signalling and mitochondrial function. Germline removal increases MML-1 nuclear accumulation and activity. Surprisingly, MML-1 regulates nuclear localization and activity of HLH-30/TFEB, a convergent regulator of autophagy, lysosome biogenesis and longevity, by downregulating TOR signalling via LARS-1/leucyl-transfer RNA synthase. HLH-30 also upregulates MML-1 upon germline removal. Mammalian MondoA/B and TFEB show similar mutual regulation. MML-1/MXL-2 and HLH-30 transcriptomes show both shared and preferential outputs including MDL-1/MAD-like HLH factor required for longevity. These studies reveal how an extensive interdependent HLH transcription factor network distributes responsibility and mutually enforces states geared towards reproduction or survival.

Indexed as

LongevitySignal TransductionAnimalsAutophagyBasic Helix-Loop-Helix ProteinsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell NucleusGene Expression ProfilingGene Expression RegulationGene Knockdown TechniquesGerm CellsGonadsPhosphotransferases (Alcohol Group Acceptor)Protein TransportReproductionBasic Helix-Loop-Helix ProteinsCaenorhabditis elegans ProteinsHLH-30 protein, C eleganslet-363 protein, C elegansMML-1 protein, C elegansMXL-2 protein, C elegansPhosphotransferases (Alcohol Group Acceptor)Trans-Activators

Identifiers

PMID27001890
PMCPMC4804169
OpenAlexW2330674382

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.