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Clathrin-Mediated Endocytosis Regulates a Balance between Opposing Signals to Maintain the Pluripotent State of Embryonic Stem Cells

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dc.contributor.author Narayana, Yadavalli V. en_US
dc.contributor.author Gadgil, Chetan en_US
dc.contributor.author Mote, Ridim D. en_US
dc.contributor.author RAJAN, RAGHAV en_US
dc.contributor.author Subramanyam, Deepa en_US
dc.date.accessioned 2019-01-24T09:13:27Z
dc.date.available 2019-01-24T09:13:27Z
dc.date.issued 2019-01 en_US
dc.identifier.citation Stem Cell Reports, 12(1), 152-164. en_US
dc.identifier.issn 2213-6711 en_US
dc.identifier.uri http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/1546
dc.identifier.uri https://doi.org/10.1016/j.stemcr.2018.11.018 en_US
dc.description.abstract Endocytosis is implicated in the maintenance of embryonic stem cell (ESC) pluripotency, although its exact role and the identity of molecular players remain poorly understood. Here, we show that the clathrin heavy chain (CLTC), involved in clathrin-mediated endocytosis (CME), is vital for maintaining mouse ESC (mESC) pluripotency. Knockdown of Cltc resulted in a loss of pluripotency accompanied by reduced E-cadherin (E-CAD) levels and increased levels of transforming growth factor beta (TGF-beta) and extracellular signal-regulated kinase (ERK) signaling. We demonstrate that both E-CAD and TGF-beta receptor type 1 (TGF-beta R1) are internalized through CME in mESCs. While E-CAD is recycled, TGF-beta R1 is targeted for lysosomal degradation thus maintaining inverse levels of these molecules. Finally, we show that E-CAD interacts with ERK, and that the decreased pluripotency upon CME loss can be rescued by inhibiting TGF-beta R, MEK, and GSK3 beta, or overexpressing E-CAD. Our results demonstrate that CME is critical for balancing signaling outputs to regulate ESC pluripotency, and possibly cell fate choices in early development. en_US
dc.language.iso en en_US
dc.publisher Elsevier B.V. en_US
dc.subject Embryonic stem cells en_US
dc.subject Pluripotency en_US
dc.subject Trafficking en_US
dc.subject E-cadherin en_US
dc.subject Clathrin en_US
dc.subject Recycling en_US
dc.subject TGF-β en_US
dc.subject Epithelial en_US
dc.subject TOC-JAN-2019 en_US
dc.subject 2019 en_US
dc.title Clathrin-Mediated Endocytosis Regulates a Balance between Opposing Signals to Maintain the Pluripotent State of Embryonic Stem Cells en_US
dc.type Article en_US
dc.contributor.department Dept. of Biology en_US
dc.identifier.sourcetitle Stem Cell Reports en_US
dc.publication.originofpublisher Foreign en_US


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