Evidence map›Paper›PMID 27799288›Full record

ArticleEMBO reports2016

Loss of Nat4 and its associated histone H4 N-terminal acetylation mediates calorie restriction-induced longevity.

Diego Molina-Serrano, Vassia Schiza, Christis Demosthenous, Emmanouil Stavrou, Jan Oppelt, Dimitris Kyriakou, Wei Liu, Gertrude Zisser, Helmut Bergler, Weiwei Dang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

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  13. Caloric restriction induced epigenetic effects on aging.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. New Insights into the Role of Histone Changes in Aging.International journal of molecular sciences · 2020
    Review
  18. Article
  19. Review
  20. Article
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

11 authors at 4 institutions in 4 countries.

Diego Molina-SerranoDepartment of Biological Sciences, University of Cyprus, Nicosia, Cyprus.ORCID 0000-0002-3961-5382
Vassia SchizaDepartment of Biological Sciences, University of Cyprus, Nicosia, Cyprus.
Christis DemosthenousDepartment of Biological Sciences, University of Cyprus, Nicosia, Cyprus.
Emmanouil StavrouDepartment of Biological Sciences, University of Cyprus, Nicosia, Cyprus.
Jan OppeltCEITEC-Central European Institute of Technology, Masaryk University, Brno, Czech Republic.
Dimitris KyriakouDepartment of Biological Sciences, University of Cyprus, Nicosia, Cyprus.
Wei LiuHuffington Center on Aging, Baylor College of Medicine, Houston, TX, USA.
Gertrude ZisserInstitut für Molekulare Biowissenschaften, Karl-Franzens-Universität, Graz, Austria.
Helmut BerglerInstitut für Molekulare Biowissenschaften, Karl-Franzens-Universität, Graz, Austria.
Weiwei DangHuffington Center on Aging, Baylor College of Medicine, Houston, TX, USA.
Antonis KirmizisDepartment of Biological Sciences, University of Cyprus, Nicosia, Cyprus kirmizis@ucy.ac.cy.ORCID 0000-0002-3748-8711
University of Cyprus · CYBaylor College of Medicine · USUniversity of Graz · ATCentral European Institute of Technology · CZ

Funding

European Research Council 260797
6 · The paper itself

Abstract

Changes in histone modifications are an attractive model through which environmental signals, such as diet, could be integrated in the cell for regulating its lifespan. However, evidence linking dietary interventions with specific alterations in histone modifications that subsequently affect lifespan remains elusive. We show here that deletion of histone N-alpha-terminal acetyltransferase Nat4 and loss of its associated H4 N-terminal acetylation (N-acH4) extend yeast replicative lifespan. Notably, nat4Δ-induced longevity is epistatic to the effects of calorie restriction (CR). Consistent with this, (i) Nat4 expression is downregulated and the levels of N-acH4 within chromatin are reduced upon CR, (ii) constitutive expression of Nat4 and maintenance of N-acH4 levels reduces the extension of lifespan mediated by CR, and (iii) transcriptome analysis indicates that nat4Δ largely mimics the effects of CR, especially in the induction of stress-response genes. We further show that nicotinamidase Pnc1, which is typically upregulated under CR, is required for nat4Δ-mediated longevity. Collectively, these findings establish histone N-acH4 as a regulator of cellular lifespan that links CR to increased stress resistance and longevity.

Indexed as

Caloric RestrictionGene Expression Regulation, FungalAcetylationChromatinDown-RegulationGene Expression ProfilingHistone AcetyltransferasesHistonesLongevityNicotinamidaseN-Terminal Acetyltransferase DProtein Processing, Post-TranslationalSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTime FactorsTranscriptional ActivationChromatinHistone AcetyltransferasesHistonesNAT4 protein, S cerevisiaeNicotinamidaseN-Terminal Acetyltransferase DPNC1 protein, S cerevisiaeSaccharomyces cerevisiae Proteinscalorie restrictionhistone N‐terminal acetylationlifespanNat4Pnc1

Identifiers

PMID27799288
PMCPMC5167350
OpenAlexW2542444614

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.