Evidence map›Paper›PMID 24936793›Full record

ArticlePLoS biology2014

Fusion of protein aggregates facilitates asymmetric damage segregation.

Miguel Coelho, Steven J Lade, Simon Alberti, Thilo Gross, Iva M Tolić

Abstract read
In one paragraph

Article in PLoS biology, 2014. 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
–field-weighted citation impact
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.

  1. Article
  2. Balance between asymmetric allocation and repair of somatic damage in unicellular life forms as an ancient form of r/K selection.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. TheeLife · 2020
    Article
  9. Article
  10. Ends and middle: Global force balance and septum location in fission yeast.The European physical journal. E, Soft matter · 2020
    Article
  11. Protein aggregation in bacteria.FEMS microbiology reviews · 2020
    Review
  12. Microbial ageing and longevity.Nature reviews. Microbiology · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Miguel CoelhoMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany; FAS Center for Systems Biology, Harvard University, Cambridge, Massachusetts, United States of America.
Steven J LadeMax Planck Institute for the Physics of Complex Systems, Dresden, Germany; Stockholm Resilience Centre, Stockholm University, Stockholm, Sweden.
Simon AlbertiMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Thilo GrossMax Planck Institute for the Physics of Complex Systems, Dresden, Germany; Department of Engineering Mathematics, Merchant Venturers School of Engineering, University of Bristol, Bristol, United Kingdom.
Iva M TolićMax Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany; Division of Molecular Biology, Ruđer Bošković Institute, Zagreb, Croatia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asymmetric segregation of damaged proteins at cell division generates a cell that retains damage and a clean cell that supports population survival. In cells that divide asymmetrically, such as Saccharomyces cerevisiae, segregation of damaged proteins is achieved by retention and active transport. We have previously shown that in the symmetrically dividing Schizosaccharomyces pombe there is a transition between symmetric and asymmetric segregation of damaged proteins. Yet how this transition and generation of damage-free cells are achieved remained unknown. Here, by combining in vivo imaging of Hsp104-associated aggregates, a form of damage, with mathematical modeling, we find that fusion of protein aggregates facilitates asymmetric segregation. Our model predicts that, after stress, the increased number of aggregates fuse into a single large unit, which is inherited asymmetrically by one daughter cell, whereas the other one is born clean. We experimentally confirmed that fusion increases segregation asymmetry, for a range of stresses, and identified Hsp16 as a fusion factor. Our work shows that fusion of protein aggregates promotes the formation of damage-free cells. Fusion of cellular factors may represent a general mechanism for their asymmetric segregation at division.

Indexed as

Asymmetric Cell DivisionModels, BiologicalProtein AggregatesAdenosine TriphosphatasesHeat-Shock ProteinsSchizosaccharomycesSchizosaccharomyces pombe ProteinsStress, PhysiologicalAdenosine TriphosphatasesHeat-Shock ProteinsHSP104 protein, S pombeProtein AggregatesSchizosaccharomyces pombe Proteins

Identifiers

PMID24936793
PMCPMC4061010

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.