Evidence map›Paper›PMID 34831384›Full record

ArticleCells2021

Phosphate Restriction Promotes Longevity via Activation of Autophagy and the Multivesicular Body Pathway.

Mahsa Ebrahimi, Lukas Habernig, Filomena Broeskamp, Andreas Aufschnaiter, Jutta Diessl, Isabel Atienza, Steffen Matz, Felix A Ruiz, Sabrina Büttner

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. NADCells · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Quiescence inAnnual review of genetics · 2022
    Review
  14. Article
  15. 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

9 authors at 3 institutions in 3 countries.

Mahsa EbrahimiDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.
Lukas HabernigDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.
Filomena BroeskampDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.ORCID 0000-0002-6955-3901
Andreas AufschnaiterDepartment of Biochemistry and Biophysics, Stockholm University, 106 91 Stockholm, Sweden.ORCID 0000-0001-6571-2162
Jutta DiesslDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.ORCID 0000-0002-4044-5413
Isabel AtienzaInstituto de Investigación e Innovación Biomédica de Cádiz (INIBICA), University of Cadiz, 11001 Cadiz, Spain.
Steffen MatzDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.
Felix A RuizInstituto de Investigación e Innovación Biomédica de Cádiz (INIBICA), University of Cadiz, 11001 Cadiz, Spain.ORCID 0000-0003-0748-5015
Sabrina BüttnerDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.ORCID 0000-0002-2786-8542
Stockholm University · SEUniversidad de Cádiz · ESUniversity of Graz · AT

Funding

Austrian Science Fund FWF J 4398
6 · The paper itself

Abstract

Nutrient limitation results in an activation of autophagy in organisms ranging from yeast, nematodes and flies to mammals. Several evolutionary conserved nutrient-sensing kinases are critical for efficient adaptation of yeast cells to glucose, nitrogen or phosphate depletion, subsequent cell-cycle exit and the regulation of autophagy. Here, we demonstrate that phosphate restriction results in a prominent extension of yeast lifespan that requires the coordinated activity of autophagy and the multivesicular body pathway, enabling efficient turnover of cytoplasmic and plasma membrane cargo. While the multivesicular body pathway was essential during the early days of aging, autophagy contributed to long-term survival at later days. The cyclin-dependent kinase Pho85 was critical for phosphate restriction-induced autophagy and full lifespan extension. In contrast, when cell-cycle exit was triggered by exhaustion of glucose instead of phosphate, Pho85 and its cyclin, Pho80, functioned as negative regulators of autophagy and lifespan. The storage of phosphate in form of polyphosphate was completely dispensable to in sustaining viability under phosphate restriction. Collectively, our results identify the multifunctional, nutrient-sensing kinase Pho85 as critical modulator of longevity that differentially coordinates the autophagic response to distinct kinds of starvation.

Indexed as

AutophagyCyclin-Dependent KinasesLongevityMultivesicular BodiesPhosphatesPolyphosphatesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCyclin-Dependent KinasesPHO85 protein, S cerevisiaePhosphatesPolyphosphatesSaccharomyces cerevisiae Proteinsagingautophagylifespannutrient limitationPho85polyphosphatequiescencevacuole fusionyeast

Identifiers

PMID34831384
PMCPMC8620443
OpenAlexW3213968997

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.