A1 Refereed original research article in a scientific journal
Integrin β1 activity controls colony morphology during human pluripotent stem cell state transitions
Authors: Taskinen, Maria E.; Pasquier, Nicolas; Stubb, Aki; Joshi, Shreya; Chastney, Megan R.; Rasila, Paula; Vahlman, Sonja; Sokka, Joonas; Lönnberg, Tapio; Mikkola, Lea; Trokovic, Ras; Ivaska, Johanna
Publisher: Elsevier BV
Publication year: 2025
Journal: Stem Cell Reports
Journal name in source: Stem Cell Reports
Article number: 102538
eISSN: 2213-6711
DOI: https://doi.org/10.1016/j.stemcr.2025.102538
Web address : https://doi.org/10.1016/j.stemcr.2025.102538
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/498548385
Integrin β1-mediated adhesion is dispensable in early mouse embryogenesis (pre-implantation) but indispensable post-implantation, suggesting distinct roles for β1-integrin-mediated adhesions in the naive (pre-implantation) versus primed (post-implantation) pluripotent stem cells (PSCs). We investigated the role of integrin β1 in regulating naive-like and primed human induced PSC (hiPSC) states. We find that integrin β1 is active in both in vitro. In primed hiPSCs, integrin β1 inhibition induces naive-like colony features, reduces actomyosin contraction and extracellular signal-regulated kinase (ERK) activity, and alters gene expression, indicative of more naive-like features. These resemble the dramatic reorganization of the colony morphology, actin cytoskeleton, and adhesions upon chemical reversion from primed to naive states of pluripotency. Importantly, functional and single-cell transcriptomics analyses demonstrate that integrin β1 inhibition attenuates colony morphology transitions in cells exiting naive pluripotency. These data reveal unprecedented integrin-dependent regulation of PSC states and demonstrate how integrin inhibitors may help to fine-tune hiPSC function and properties in vitro.
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Funding information in the publication:
This study was supported by the Research Council of Finland (J.I. 330033; 325464), Research Council of Finland CoE in Cell and Tissue Mechanics (J.I. 364182), InFLAMES Flagship Programme of the Research Council of Finland (decision number: 337530), the Sigrid Juselius Foundation (J.I.), and European Research Council Advanced Grant (101142305). M.E.T. has been supported by the University of Turku Doctoral Program for Molecular Medicine, Finnish Cultural Foundation, K. Albin Johansson Foundation, and Magnus Ehrnrooth Foundation. N.P. has been supported by the “PhD in Oncology” program from the Philantropia Foundation and the Turku University Foundation. S.J. has been supported by the Turku University Foundation. J.S. and R.T. have been supported by the Jane and Aatos Erkko Foundation.
