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Updated: May 21, 2025
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An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
Published on: December 3, 2020
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Epigenetic fluidity meets phenotypic malleability in intestinal epithelial cells
Swarnabh Bhattacharya1, Ramesh A Shivdasani1
1Department of Medical Oncology and Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
Cell Chemical Biology
|March 21, 2025
Summary
Differentiated intestinal cells can regain stem cell properties when needed. Research shows H3K36 methylation helps maintain cell identity, controlling tissue regeneration and plasticity.
Area of Science:
- Cell biology
- Stem cell biology
- Epigenetics
Background:
- Intestinal stem cells (ISCs) are crucial for tissue homeostasis and regeneration.
- Differentiated progenitor cells in intestinal crypts can revert to a multipotent state in response to stem cell loss.
- Understanding the mechanisms that regulate this cellular plasticity is vital for regenerative medicine.
Purpose of the Study:
- To investigate the epigenetic mechanisms that maintain differentiated cell states in the intestinal epithelium.
- To identify factors that regulate the plasticity of intestinal progenitor cells.
Main Methods:
- Chromatin immunoprecipitation sequencing (ChIP-seq) to analyze H3K36 methylation patterns.
- Gene expression analysis to assess the impact of H3K36 methylation on cell-type-restricted genes.
- In vivo studies in mouse models of intestinal injury.
Main Results:
- H3K36 methylation is enriched at cell-type-restricted genes in differentiated intestinal progenitors.
- Depletion of H3K36 methylation leads to dedifferentiation and loss of cell identity.
- H3K36 methylation is essential for suppressing the multipotent state in differentiated cells.
Conclusions:
- H3K36 methylation plays a critical role in maintaining differentiated cell states within the intestinal crypts.
- This epigenetic mark acts as a barrier to dedifferentiation, thereby regulating cell plasticity and tissue regenerative capacity.
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