Evidence map›Paper›PMID 26450797›Full record

ArticleDevelopment, growth & differentiation2015

Par-aPKC-dependent and -independent mechanisms cooperatively control cell polarity, Hippo signaling, and cell positioning in 16-cell stage mouse embryos.

Yoshikazu Hirate, Shino Hirahara, Ken-Ichi Inoue, Hiroshi Kiyonari, Hiroshi Niwa, Hiroshi Sasaki

Abstract read
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Article in Development, growth & differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

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0cells of the map it votes in
49citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

49 citing papers in PubMed.

  1. Article
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  9. Origin and development of primary animal epithelia.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  10. Article
  11. Article
  12. Article
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  14. Review
  15. Journey of the mouse primitive endoderm: from specification to maturation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Emerging Role of Mechanical Forces in Cell Fate Acquisition.Frontiers in cell and developmental biology · 2022
    Review
  20. Chromatin as a sensor of metabolic changes during early development.Frontiers in cell and developmental biology · 2022
    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.

Yoshikazu HirateDepartment of Cell Fate Control, Institute of Molecular Embryology and Genetics, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811, Japan.ORCID http://orcid.org/0000-0001-9116-3603
Shino HiraharaLaboratory for Embryonic Induction, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Ken-Ichi InoueAnimal Resource Development Unit, Division of Bio-function Dynamics Imaging, RIKEN Center for Life Science Technologies, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Hiroshi KiyonariAnimal Resource Development Unit, Division of Bio-function Dynamics Imaging, RIKEN Center for Life Science Technologies, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Hiroshi NiwaLaboratory for Pluripotent Cell Studies, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Hiroshi SasakiDepartment of Cell Fate Control, Institute of Molecular Embryology and Genetics, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto, 860-0811, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In preimplantation mouse embryos, the Hippo signaling pathway plays a central role in regulating the fates of the trophectoderm (TE) and the inner cell mass (ICM). In early blastocysts with more than 32 cells, the Par-aPKC system controls polarization of the outer cells along the apicobasal axis, and cell polarity suppresses Hippo signaling. Inactivation of Hippo signaling promotes nuclear accumulation of a coactivator protein, Yap, leading to induction of TE-specific genes. However, whether similar mechanisms operate at earlier stages is not known. Here, we show that slightly different mechanisms operate in 16-cell stage embryos. Similar to 32-cell stage embryos, disruption of the Par-aPKC system activated Hippo signaling and suppressed nuclear Yap and Cdx2 expression in the outer cells. However, unlike 32-cell stage embryos, 16-cell stage embryos with a disrupted Par-aPKC system maintained apical localization of phosphorylated Ezrin/Radixin/Moesin (p-ERM), and the effects on Yap and Cdx2 were weak. Furthermore, normal 16-cell stage embryos often contained apolar cells in the outer position. In these cells, the Hippo pathway was strongly activated and Yap was excluded from the nuclei, thus resembling inner cells. Dissociated blastomeres of 8-cell stage embryos form polar-apolar couplets, which exhibit different levels of nuclear Yap, and the polar cell engulfed the apolar cell. These results suggest that cell polarization at the 16-cell stage is regulated by both Par-aPKC-dependent and -independent mechanisms. Asymmetric cell division is involved in cell polarity control, and cell polarity regulates cell positioning and most likely controls Hippo signaling.

Indexed as

AnimalsBlastocystBlastomeresCell DifferentiationCell PolarityEmbryo, MammalianFemaleGene Expression Regulation, DevelopmentalHippo Signaling PathwayHomeodomain ProteinsMicePregnancyProtein Kinase CProtein Serine-Threonine KinasesSignal TransductionHomeodomain ProteinsProtein Kinase CProtein Serine-Threonine Kinasesasymmetric cell divisioncell polarityHippo signalingPar-aPKCpreimplantation embryo

Identifiers

PMID26450797
PMCPMC11520972

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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.