Evidence map›Paper›PMID 28737772›Full record

ArticleNature cell biology2017

Cortical forces and CDC-42 control clustering of PAR proteins for Caenorhabditis elegans embryonic polarization.

Shyi-Chyi Wang, Tricia Yu Feng Low, Yukako Nishimura, Laurent Gole, Weimiao Yu, Fumio Motegi

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In one paragraph

Article in Nature cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
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  6. A PDZ-kinase allosteric relay mediates Par complex regulator exchange.bioRxiv : the preprint server for biology · 2024
    Article
  7. Article
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  11. Article
  12. Article
  13. Review
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  15. Myosin turnover controls actomyosin contractile instability.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Article
  17. Review
  18. Advances in the study of CDC42 in the female reproductive system.Journal of cellular and molecular medicine · 2022
    Review
  19. Article
  20. 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

6 authors at 3 institutions in 2 countries.

Shyi-Chyi WangTemasek Life-sciences Laboratory, 1 Research Link, National University of Singapore, Singapore 117604, Singapore.
Tricia Yu Feng LowTemasek Life-sciences Laboratory, 1 Research Link, National University of Singapore, Singapore 117604, Singapore.
Yukako NishimuraMechanobiology Institute, National University of Singapore, T-Lab, 5A Engineering Drive 1, Singapore 117411, Singapore.
Laurent GoleInstitute for Molecular and Cell Biology, Agency for Science Technology and Research, 61 Biopolis Drive, Singapore 138673, Singapore.
Weimiao YuInstitute for Molecular and Cell Biology, Agency for Science Technology and Research, 61 Biopolis Drive, Singapore 138673, Singapore.ORCID http://orcid.org/0000-0001-5092-1009
Fumio MotegiTemasek Life-sciences Laboratory, 1 Research Link, National University of Singapore, Singapore 117604, Singapore.ORCID http://orcid.org/0000-0001-9058-6559
Temasek Life Sciences Laboratory · SGAgency for Science, Technology and Research · SGNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell polarization enables zygotes to acquire spatial asymmetry, which in turn patterns cellular and tissue axes during development. Local modification in the actomyosin cytoskeleton mediates spatial segregation of partitioning-defective (PAR) proteins at the cortex, but how mechanical changes in the cytoskeleton are transmitted to PAR proteins remains elusive. Here we uncover a role of actomyosin contractility in the remodelling of PAR proteins through cortical clustering. During embryonic polarization in Caenorhabditis elegans, actomyosin contractility and the resultant cortical tension stimulate clustering of PAR-3 at the cortex. Clustering of atypical protein kinase C (aPKC) is supported by PAR-3 clusters and is antagonized by activation of CDC-42. Cortical clustering is associated with retardation of PAR protein exchange at the cortex and with effective entrainment of advective cortical flows. Our findings delineate how cytoskeleton contractility couples the cortical clustering and long-range displacement of PAR proteins during polarization. The principles described here would apply to other pattern formation processes that rely on local modification of cortical actomyosin and PAR proteins.

Indexed as

Cell PolarityMechanotransduction, CellularActomyosinAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsCell Cycle ProteinsCytoskeletonEmbryo, NonmammalianGene Expression Regulation, DevelopmentalGenotypeGTP-Binding ProteinsMembrane ProteinsMiceMicroscopy, FluorescenceActomyosinCaenorhabditis elegans Proteinscdc-42 protein, C elegansCell Cycle ProteinsGTP-Binding ProteinsMembrane ProteinsPAR-3 protein, C elegansPKC-3 proteinProtein Kinase CProtein Serine-Threonine Kinases

Identifiers

PMID28737772
OpenAlexW2737413500

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.