Evidence map›Paper›PMID 26804466›Full record

ArticleScientific reports2016

Glucose restriction induces transient G2 cell cycle arrest extending cellular chronological lifespan.

Fumie Masuda, Mahiro Ishii, Ayaka Mori, Lisa Uehara, Mitsuhiro Yanagida, Kojiro Takeda, Shigeaki Saitoh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

  1. Sugar signals pedal the cell cycle!Frontiers in plant science · 2024
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  10. Extension of chronological lifespan in Schizosaccharomyces pombe.Genes to cells : devoted to molecular & cellular mechanisms · 2021
    Review
  11. Article
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  15. Article
  16. The HIV-1 Vpr Protein: A Multifaceted Target for Therapeutic Intervention.International journal of molecular sciences · 2017
    Review
  17. 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

7 authors at 3 institutions in 1 country.

Fumie MasudaInstitute of Life Science, Kurume University, Hyakunen-Khoen 1-1, Kurume, Fukuoka 839-0864, Japan.
Mahiro IshiiDepartment of Biology, Faculty of Science and Engineering, Konan University, 8-9-1 Okamoto, Higashinada-ku, Kobe 658-8501, Japan.
Ayaka MoriOkinawa Institute of Science and Technology Graduate School, Tancha 1919-1, Onna, Okinawa 904-0495, Japan.
Lisa UeharaOkinawa Institute of Science and Technology Graduate School, Tancha 1919-1, Onna, Okinawa 904-0495, Japan.
Mitsuhiro YanagidaOkinawa Institute of Science and Technology Graduate School, Tancha 1919-1, Onna, Okinawa 904-0495, Japan.
Kojiro TakedaDepartment of Biology, Faculty of Science and Engineering, Konan University, 8-9-1 Okamoto, Higashinada-ku, Kobe 658-8501, Japan.
Shigeaki SaitohInstitute of Life Science, Kurume University, Hyakunen-Khoen 1-1, Kurume, Fukuoka 839-0864, Japan.
Okinawa Institute of Science and Technology Graduate University · JPKonan University · JPKurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While glucose is the fundamental source of energy in most eukaryotes, it is not always abundantly available in natural environments, including within the human body. Eukaryotic cells are therefore thought to possess adaptive mechanisms to survive glucose-limited conditions, which remain unclear. Here, we report a novel mechanism regulating cell cycle progression in response to abrupt changes in extracellular glucose concentration. Upon reduction of glucose in the medium, wild-type fission yeast cells undergo transient arrest specifically at G2 phase. This cell cycle arrest is dependent on the Wee1 tyrosine kinase inhibiting the key cell cycle regulator, CDK1/Cdc2. Mutant cells lacking Wee1 are not arrested at G2 upon glucose limitation and lose viability faster than the wild-type cells under glucose-depleted quiescent conditions, suggesting that this cell cycle arrest is required for extension of chronological lifespan. Our findings indicate the presence of a novel cell cycle checkpoint monitoring glucose availability, which may be a good molecular target for cancer therapy.

Indexed as

CDC2 Protein KinaseCell Cycle ProteinsCell DivisionCulture MediaDNA DamageG2 Phase Cell Cycle CheckpointsGene Expression Regulation, FungalGlucoseHumansNuclear ProteinsPhosphorylationProtein-Tyrosine KinasesSchizosaccharomycesSchizosaccharomyces pombe ProteinsCDC2 Protein KinaseCell Cycle ProteinsCulture MediaGlucoseNuclear ProteinsProtein-Tyrosine KinasesSchizosaccharomyces pombe Proteinswee1 protein, S pombe

Identifiers

PMID26804466
PMCPMC4726166
OpenAlexW2415167083

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.