Evidence map›Paper›PMID 22084378›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2011

Nutrient limitations alter cell division control and chromosome segregation through growth-related kinases and phosphatases.

Mitsuhiro Yanagida, Nobuyasu Ikai, Mizuki Shimanuki, Kenichi Sajiki

Open access · hybridAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
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

33 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. TheCells · 2025
    Article
  3. Article
  4. Relevance of Nutrient-Sensing in the Pathogenesis ofFrontiers in fungal biology · 2022
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Cellular logistics · 2017
    Article
  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

4 authors at 1 institution in 1 country.

Mitsuhiro YanagidaThe G0 Cell Unit, Okinawa Institute of Science and Technology Promotion Corporation, Tancha 1919-1, Onna, Okinawa 904-0412, Japan. myanagid@gmail.com
Nobuyasu Ikai
Mizuki Shimanuki
Kenichi Sajiki
Okinawa Institute of Science and Technology Graduate University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In dividing fission yeast Schizosaccharomyces pombe cells, the balance between Wee1 kinase and Cdc25 phosphatase which control the cyclin-dependent kinase (CDK) at the G2-M transition determines the rod-shaped cell length. Under nitrogen source starvation or glucose limitation, however, cell size determination is considerably modulated, and cell size shortening occurs for wild-type cells. For several mutants of kinases or phosphatases, including CDK, target of rapamycin complex (TORC) 1 and 2, stress-responsive mitogen-activated protein kinase (MAPK) Sty1/Spc1, MAPK kinase Wis1, calcium- and calmodulin-dependent protein kinase kinase-like Ssp1, and type 2A and 2A-related phosphatases inhibitor Sds23, this cell shortening does not normally occur. In tor1 and ssp1 mutants, cell elongation is observed. Sds23 that binds to and inhibits 2A and 2A-related phosphatases is synergistic with Ssp1 in the cell size determination and survival under low glucose and nitrogen source. Tor2 (TORC1) is required for growth, whereas Tor1 (TORC2) is needed for determining division size according to different nutrient conditions. Surprisingly, in growth-diminished tor2 mutant or rapamycin-treated cells, the requirement of separase/Cut1-securin/Cut2 essential for chromosome segregation is greatly alleviated. By contrast, defects of tor1 with secruin/cut2 or overproduction of Cut1 are additive. While Tor1 and Tor2 are opposite in their apparent functions, both may actually coordinate cell division with growth in response to the changes in nutrients.

Indexed as

Cell DivisionChromosome SegregationCell Cycle ProteinsCell Growth ProcessesEndopeptidasesGlucoseNitrogenPhenotypePhosphoprotein PhosphatasesProtein BindingProtein-Tyrosine KinasesSchizosaccharomycesSeparaseSirolimusCell Cycle ProteinsEndopeptidasesGlucoseNitrogenPhosphoprotein PhosphatasesProtein-Tyrosine KinasesSeparaseSirolimus

Identifiers

PMID22084378
PMCPMC3203466
OpenAlexW2113861872

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.