β-Catenin in Pluripotency

Sineva, G S; Поспелов, В. А.

doi:10.1016/b978-0-12-800178-3.00002-6

Cited by 25 publications

(5 citation statements)

References 103 publications

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“…It is noteworthy that the inactivation of PI3K/Akt signaling by cell surface syntaxin-4 occurred even in the presence of LIF, suggesting that the effect of syntaxin-4 might be dominant over LIF-triggered PI3K/Akt activation. Moreover, as GSK3β is a component of Wnt signaling, its subsequent activation may also affect the fate of β-catenin45. Thus, the elimination of E-cadherin might be accompanied by changes in subcellular localization or stability of β-catenin, a potent transcriptional activator for P-cadherin46.…”

Section: Discussionmentioning

confidence: 99%

Membrane translocation of t-SNARE protein syntaxin-4 abrogates ground-state pluripotency in mouse embryonic stem cells

Hagiwara-Chatani

Shirai

Kido

et al. 2017

Sci Rep

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Embryonic stem (ES) and induced pluripotent stem (iPS) cells are attractive tools for regenerative medicine therapies. However, aberrant cell populations that display flattened morphology and lose ground-state pluripotency often appear spontaneously, unless glycogen synthase kinase 3β (GSK3β) and mitogen-activated protein kinase kinase (MEK1/2) are inactivated. Here, we show that membrane translocation of the t-SNARE protein syntaxin-4 possibly is involved in this phenomenon. We found that mouse ES cells cultured without GSK3β/MEK1/2 inhibitors (2i) spontaneously extrude syntaxin-4 at the cell surface and that artificial expression of cell surface syntaxin-4 induces appreciable morphological changes and mesodermal differentiation through dephosphorylation of Akt. Transcriptome analyses revealed several candidate elements responsible for this, specifically, an E-to P-cadherin switch and a marked downregulation of Zscan4 proteins, which are DNA-binding proteins essential for ES cell pluripotency. Embryonic carcinoma cell lines F9 and P19CL6, which maintain undifferentiated states independently of Zscan4 proteins, exhibited similar cellular behaviors upon stimulation with cell surface syntaxin-4. The functional ablation of E-cadherin and overexpression of P-cadherin reproduced syntaxin-4-induced cell morphology, demonstrating that the E- to P-cadherin switch executes morphological signals from cell surface syntaxin-4. Thus, spontaneous membrane translocation of syntaxin-4 emerged as a critical element for maintenance of the stem-cell niche.

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Section: Discussionmentioning

confidence: 99%

Membrane translocation of t-SNARE protein syntaxin-4 abrogates ground-state pluripotency in mouse embryonic stem cells

Hagiwara-Chatani

Shirai

Kido

et al. 2017

Sci Rep

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“…Two prominent branches of the WNT signalling network are the so-called canonical WNT–β-catenin and non-canonical WNT–planar cell polarity (PCP) pathways. In the canonical pathway, WNT ligands bind to frizzled to trigger complex formation with the co-receptor LRP5/6 and Dishevelled (DVL), promoting stabilization of cytoplasmic β‐catenin, which enters the nucleus to regulate target gene expression with effects on cell proliferation, differentiation and survival 186, 187 . By contrast, WNT–PCP signalling regulates cell morphology, migration and oriented cell division and relies on a multitude of receptor combinations and downstream signalling events 188, 189 .…”

Section: Ciliary Modulation Of Wnt Signallingmentioning

confidence: 99%

Cellular signalling by primary cilia in development, organ function and disease

et al. 2019

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Primary cilia project in a single copy from the surface of most vertebrate cell types; they detect and transmit extracellular cues to regulate diverse cellular processes during development and to maintain tissue homeostasis. The sensory capacity of primary cilia relies on the coordinated trafficking and temporal localization of specific receptors and associated signal transduction modules in the cilium. The canonical hedgehog (HH) pathway, for example, is a bona fide ciliary signalling system that regulates cell fate and self-renewal in development and tissue homeostasis. Specific receptors and associated signal transduction proteins can also localize to primary cilia in a cell type-dependent manner; available evidence suggests that the ciliary constellation of these proteins can temporally change to allow the cell to adapt to specific developmental and homeostatic cues. Consistent with important roles for primary cilia in signalling, mutations that lead to their dysfunction underlie a pleiotropic group of diseases and syndromic disorders termed ciliopathies, which affect many different tissues and organs of the body. In this review we highlight central mechanisms by which primary cilia coordinate HH, G-protein-coupled receptor, WNT, receptor tyrosine kinase and TGFβ/BMP signalling, and illustrate how defects in the balanced output of ciliary signalling events are coupled to developmental disorders and disease progression. Opening section The primary cilium is a microtubule-based, non-motile organelle that extends as a solitary unit from the basal body (derived from the centrosomal mother centriole of most cell types

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“…Binding to the Frizzled (Fzd) receptor, which leads to complex formation with the coreceptors LRP5/6 and Disheveled (DVL). As a result, β-catenin is stabilized and translocates to the nucleus to regulate gene expression (Kim et al, 2013;Sineva and Pospelov, 2014).…”

Section: Wnt/cateninmentioning

confidence: 99%