Embryonic stem cells are devoid of macropinocytosis, a trafficking pathway for activin A in differentiated cells-Reference-Cited by-同舟云学术

Embryonic stem cells are devoid of macropinocytosis, a trafficking pathway for activin A in differentiated cells

Published:2021-07-01 Issue:13 Volume:134 Page:
ISSN:0021-9533
Container-title:Journal of Cell Science
language:en
Short-container-title:

Author:

Kostopoulou Nikoleta¹^ORCID,Bellou Sofia¹²^ORCID,Bagli Eleni¹^ORCID,Markou Maria¹³^ORCID,Kostaras Eleftherios¹³^ORCID,Hyvönen Marko⁴^ORCID,Kalaidzidis Yiannis⁵^ORCID,Papadopoulos Angelos¹⁶^ORCID,Chalmantzi Varvara¹⁶^ORCID,Kyrkou Athena¹^ORCID,Panopoulou Ekaterini³,Fotsis Theodore¹³^ORCID,Murphy Carol¹⁶⁷^ORCID

Affiliation:

1. Foundation for Research & Technology-Hellas (FORTH), Institute of Molecular Biology and Biotechnology (IMBB), Department of Biomedical Research, Ioannina, 45110, Greece

2. Confocal Laser Scanning Microscopy Unit, Network of Research Supporting Laboratories, University of Ioannina, Ioannina, 45110, Greece

3. Laboratory of Biological Chemistry, University of Ioannina Medical School, Ioannina, 45110, Greece

4. Department of Biochemistry, University of Cambridge, Cambridge, CB2 1TN, UK

5. Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany

6. School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

7. Centre of Membrane Proteins and Receptors, University of Birmingham, A118 Aston Webb, Edgbaston, Birmingham, B15 2TT, UK

Abstract

ABSTRACT Ligand–receptor complexes formed at the plasma membrane are internalised via various endocytic pathways that influence the ultimate signalling output by regulating the selection of interaction partners by the complex along the trafficking route. We report that, in differentiated cells, activin A–receptor complexes are internalised via clathrin-mediated endocytosis (CME) and macropinocytosis (MP), whereas in human embryonic stem cells (hESCs) internalisation occurs via CME. We further show that hESCs are devoid of MP, which becomes functional upon differentiation towards endothelial cells through mesoderm mediators. Our results reveal, for the first time, that MP is an internalisation route for activin A in differentiated cells, and that MP is not active in hESCs and is induced as cells differentiate.

Funder

Sixth Framework Programme

National Strategic Reference Framework

Publisher

The Company of Biologists

Subject

Cell Biology

Link

http://journals.biologists.com/jcs/article-pdf/doi/10.1242/jcs.246892/2080586/jcs246892.pdf

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