A Semi-automated Organoid Screening Method Demonstrates Epigenetic Control of Intestinal Epithelial Differentiation

Jenny Ostrop1, Rosalie T. Zwiggelaar1, Marianne Terndrup Pedersen2,3, François Gerbe4, Korbinian Bösl5, Håvard T. Lindholm1, Alberto Díez-Sánchez1, N. Parmar1, Silke Radetzki6, Jens Peter von Kries6, Philippe Jay4, Kim B. Jensen2,3, C.H. Arrowsmith7,8,9, Menno J. Oudhoff1
1Centre of Molecular Inflammation Research (CEMIR), Department of Clinical and Molecular Medicine (IKOM), NTNU - Norwegian University of Science and Technology, Trondheim, Norway
2BRIC - Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark
3Novo Nordisk Foundation Center for Stem Cell Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
4Cancer Biology Department, Institute of Functional Genomics, University of Montpellier, Montpellier, France
5Department of Bioinformatics, Computational Biological Unit, University of Bergen, Bergen, Norway
6Screening Unit, Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Berlin, Germany
7Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada
8Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada
9Structural Genomics Consortium, University of Toronto, Toronto, ON, Canada

Tóm tắt

Intestinal organoids are an excellent model to study epithelial biology. Yet, the selection of analytical tools to accurately quantify heterogeneous organoid cultures remains limited. Here, we developed a semi-automated organoid screening method, which we applied to a library of highly specific chemical probes to identify epigenetic regulators of intestinal epithelial biology. The role of epigenetic modifiers in adult stem cell systems, such as the intestinal epithelium, is still undefined. Based on this resource dataset, we identified several targets that affected epithelial cell differentiation, including HDACs, EP300/CREBBP, LSD1, and type I PRMTs, which were verified by complementary methods. For example, we show that inhibiting type I PRMTs, which leads enhanced epithelial differentiation, blocks the growth of adenoma but not normal organoid cultures. Thus, epigenetic probes are powerful tools to study intestinal epithelial biology and may have therapeutic potential.

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