Related Experiment Video

Updated: May 21, 2026

Oct4GiP Reporter Assay to Study Genes that Regulate Mouse Embryonic Stem Cell Maintenance and Self-renewal
08:01

Oct4GiP Reporter Assay to Study Genes that Regulate Mouse Embryonic Stem Cell Maintenance and Self-renewal

Published on: May 30, 2012

E-cadherin and, in its absence, N-cadherin promotes Nanog expression in mouse embryonic stem cells via STAT3

Kate Hawkins1, Lisa Mohamet, Sarah Ritson

  • 1Stem Cell Biology Group, Core Technology Facility, The University of Manchester, Manchester, United Kingdom.

Stem Cells (Dayton, Ohio)
|June 15, 2012
PubMed

Insights

E-cadherin maintains mouse embryonic stem cell pluripotency by promoting Klf4 and Nanog expression through STAT3 phosphorylation. N-cadherin supports this function, revealing a novel cadherin-pluripotency circuitry.

Area of Science:

  • Stem cell biology
  • Molecular and cell biology
  • Developmental biology

Background:

  • E-cadherin loss in mouse embryonic stem cells (mESCs) alters transcriptome and pluripotency signaling pathways.
  • E-cadherin is crucial for maintaining pluripotency in mESCs.

Purpose of the Study:

  • To elucidate the molecular mechanism by which E-cadherin regulates pluripotency in mESCs.
  • To investigate the role of E-cadherin and N-cadherin in leukemia inhibitory factor (LIF)-dependent pluripotency.

Main Methods:

  • Culture of E-cadherin null (Ecad(-/-)) mESCs in supplemented medium.
  • Analysis of transcript and protein expression (Klf4, Nanog, N-cadherin).
  • Assessment of STAT3 phosphorylation and cell-cell contact restoration.
  • Abrogation of N-cadherin using an inhibitory peptide.

Main Results:

  • E-cadherin promotes Klf4 and Nanog expression via STAT3 phosphorylation, requiring β-catenin.
  • Ecad(-/-) mESCs partially restore cell-cell contact, STAT3 phosphorylation, and upregulate Klf4, Nanog, and N-cadherin in LIF/BMP medium.
  • N-cadherin supports LIF-dependent pluripotency; its abrogation leads to loss of phospho STAT3, Klf4, and Nanog.

Conclusions:

  • A novel molecular mechanism links E-cadherin and N-cadherin to the core pluripotency circuitry in mESCs.
  • This mechanism may explain E-cadherin's role in induced pluripotent stem cell reprogramming.
  • Cadherin-mediated cell adhesion is critical for maintaining stem cell pluripotency.

More Related Videos

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells09:32

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells

Published on: February 27, 2020

Differentiation of Mouse Embryonic Stem Cells into Cortical Interneuron Precursors10:24

Differentiation of Mouse Embryonic Stem Cells into Cortical Interneuron Precursors

Published on: December 3, 2017

Related Concept Videos

Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
Catenins01:23

Catenins

Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
Catenins in Cell Junctions
Catenins bind to cell adhesion molecules such as cadherins and link them to different cytoskeletal proteins depending on the type of cell junction. At the adherens...
Structure of Cadherins01:25

Structure of Cadherins

The cadherins were one of the first cell adhesion molecules discovered; the term “cadherins”   is based on their calcium-dependent adhering properties. The first cadherins discovered on the epithelial, neuronal, and placental cells were named E-cadherin, P-cadherin, and N-cadherin, respectively. These classical cadherins share sequence and structural similarities. Other cadherins, including those involved in cell signaling, are grouped into non-classical cadherins. This diversity of cadherins...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...