Evidence map›Paper›PMID 21966261›Full record

ArticlePLoS computational biology2011

Filament depolymerization can explain chromosome pulling during bacterial mitosis.

Edward J Banigan, Michael A Gelbart, Zemer Gitai, Ned S Wingreen, Andrea J Liu

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Self-organization principles of intracellular pattern formation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018
    Review
  4. Article
  5. DNA-relay mechanism is sufficient to explain ParA-dependent intracellular transport and patterning of single and multiple cargos.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  6. Article
  7. Directed and persistent movement arises from mechanochemistry of the ParA/ParB system.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  8. Article
  9. Article
  10. Article
  11. Condensation and localization of the partitioning protein ParB on the bacterial chromosome.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Caulobacter chromosome in vivo configuration matches model predictions for a supercoiled polymer in a cell-like confinement.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  17. Article
  18. Review
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.

Edward J BaniganDepartment of Physics and Astronomy, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Michael A Gelbart
Zemer Gitai
Ned S Wingreen
Andrea J Liu
Princeton University · USUniversity of Pennsylvania · US

Funding

Discovering Antibiotic Drugs & Targets via High-Throughput Bacterial Cell BiologyDP2OD004389 · OD · PRINCETON UNIVERSITY · PI GITAI, ZEMER · 2008 to 2008
$2.4M
NIH HHS 1DP2OD004389NIH HHS DP2 OD004389
6 · The paper itself

Abstract

Chromosome segregation is fundamental to all cells, but the force-generating mechanisms underlying chromosome translocation in bacteria remain mysterious. Caulobacter crescentus utilizes a depolymerization-driven process in which a ParA protein structure elongates from the new cell pole, binds to a ParB-decorated chromosome, and then retracts via disassembly, pulling the chromosome across the cell. This poses the question of how a depolymerizing structure can robustly pull the chromosome that disassembles it. We perform Brownian dynamics simulations with a simple, physically consistent model of the ParABS system. The simulations suggest that the mechanism of translocation is "self-diffusiophoretic": by disassembling ParA, ParB generates a ParA concentration gradient so that the ParA concentration is higher in front of the chromosome than behind it. Since the chromosome is attracted to ParA via ParB, it moves up the ParA gradient and across the cell. We find that translocation is most robust when ParB binds side-on to ParA filaments. In this case, robust translocation occurs over a wide parameter range and is controlled by a single dimensionless quantity: the product of the rate of ParA disassembly and a characteristic relaxation time of the chromosome. This time scale measures the time it takes for the chromosome to recover its average shape after it is has been pulled. Our results suggest explanations for observed phenomena such as segregation failure, filament-length-dependent translocation velocity, and chromosomal compaction.

Indexed as

Models, GeneticBacterial ProteinsCaulobacter crescentusChromosomes, BacterialChromosome SegregationComputer SimulationMitosisMolecular Dynamics SimulationPolymerizationProtein BindingBacterial Proteinschromosome partition proteins, bacterial

Identifiers

PMID21966261
PMCPMC3178632
OpenAlexW2062132232

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.