Evidence map›Paper›PMID 28264932›Full record

ArticleThe Journal of biological chemistry2017

Zinc starvation induces autophagy in yeast.

Tomoko Kawamata, Tetsuro Horie, Miou Matsunami, Michiko Sasaki, Yoshinori Ohsumi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  5. Coordination chemistry suggests that independently observed benefits of metformin and ZnBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
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  11. Global Molecular Response ofJournal of fungi (Basel, Switzerland) · 2023
    Article
  12. Quiescence inAnnual review of genetics · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

5 authors at 2 institutions in 1 country.

Tomoko KawamataResearch Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503.
Tetsuro HorieResearch Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503; Research Center for Odontology, School of Life Dentistry at Tokyo, The Nippon Dental University, Chiyoda-ku, Tokyo 102-8159, Japan.
Miou MatsunamiResearch Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503.
Michiko SasakiResearch Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503.
Yoshinori OhsumiResearch Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503. Electronic address: yohsumi@iri.titech.ac.jp.
Tokyo Institute of Technology · JPNippon Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc is an essential nutrient for all forms of life. Within cells, most zinc is bound to protein. Because zinc serves as a catalytic or structural cofactor for many proteins, cells must maintain zinc homeostasis under severely zinc-deficient conditions. In yeast, the transcription factor Zap1 controls the expression of genes required for uptake and mobilization of zinc, but to date the fate of existing zinc-binding proteins under zinc starvation remains poorly understood. Autophagy is an evolutionarily conserved cellular degradation/recycling process in which cytoplasmic proteins and organelles are sequestered for degradation in the vacuole/lysosome. In this study, we investigated how autophagy functions under zinc starvation. Zinc depletion induced non-selective autophagy, which is important for zinc-limited growth. Induction of autophagy by zinc starvation was not directly related to transcriptional activation of Zap1. Instead, TORC1 inactivation directed zinc starvation-induced autophagy. Abundant zinc proteins, such as Adh1, Fba1, and ribosomal protein Rpl37, were degraded in an autophagy-dependent manner. But the targets of autophagy were not restricted to zinc-binding proteins. When cellular zinc is severely depleted, this non-selective autophagy plays a role in releasing zinc from the degraded proteins and recycling zinc for other essential purposes.

Indexed as

AutophagyAlcohol DehydrogenaseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProteolysisSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTOR Serine-Threonine KinasesTranscription FactorsZincADH1 protein, S cerevisiaeAlcohol DehydrogenaseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesSaccharomyces cerevisiae ProteinsTOR Serine-Threonine KinasesTranscription FactorsZAP1 protein, S cerevisiaeZincautophagymetalstarvationTOR complex (TORC)yeastzinc

Identifiers

PMID28264932
PMCPMC5437255
OpenAlexW2594744254

What OpenQuestion holds

Textmetadata
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.