Epigenetics in Stem Cells and Their Derivatives

A special issue of Epigenomes (ISSN 2075-4655).

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 10187

Special Issue Editor


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Guest Editor
Institut de Génomique Fonctionnelle, Université de Montpellier, INSERM, CNRS, Montpellier, France
Interests: pluripotent stem cells; genomic imprinting; organoids; brain development

Special Issue Information

Dear Colleagues,

Epigenetic modifications play a key role in the control of gene expression in stem cells.

In vivo, epigenetic modifications, including DNA methylation, histone marks, and non-coding RNAs, are instrumental for lineage commitment of stem cells during development, and for tissue repair by resident stem cells in adult tissues. In addition, epigenetic modifications participate in the loss of identify of stem cells, which accompany tumour development.

In vitro, stem cells are used as models that recapitulate in vivo development, and are a potential source of cells for therapy. However, in vitro culture has a major impact on the epigenetic signature of stem cells and on the quality of their derivatives.

In this Special Issue, we welcome review, research, and method manuscripts covering the following areas:

  • Epigenetics status of undifferentiated pluripotent stem cells, and how it compares to the in vivo situation.
  • Epigenetics status of the derivatives of pluripotent stem cells, including organoids.
  • Influence of epigenetic modifications on the developmental trajectories of stem cells.
  • Influence of epigenetic modifications on the repair capacity of tissue-specific stem cells.
  • Influence of epigenetic modifications on the loss of identity of stem cells, leading to the emergence of cancer stem cells.

Dr. Tristan Bouschet
Guest Editor

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Published Papers (2 papers)

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Research

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18 pages, 4482 KiB  
Article
Simplified MethylRAD Sequencing to Detect Changes in DNA Methylation at Enhancer Elements in Differentiating Embryonic Stem Cells
by Debapriya Saha, Allison B. Norvil, Nadia A. Lanman and Humaira Gowher
Epigenomes 2020, 4(4), 24; https://doi.org/10.3390/epigenomes4040024 - 1 Oct 2020
Cited by 4 | Viewed by 5146
Abstract
Differential DNA methylation is characteristic of gene regulatory regions, such as enhancers, which mostly constitute low or intermediate CpG content in their DNA sequence. Consequently, quantification of changes in DNA methylation at these sites is challenging. Given that DNA methylation across most of [...] Read more.
Differential DNA methylation is characteristic of gene regulatory regions, such as enhancers, which mostly constitute low or intermediate CpG content in their DNA sequence. Consequently, quantification of changes in DNA methylation at these sites is challenging. Given that DNA methylation across most of the mammalian genome is maintained, the use of genome-wide bisulfite sequencing to measure fractional changes in DNA methylation at specific sites is an overexertion which is both expensive and cumbersome. Here, we developed a MethylRAD technique with an improved experimental plan and bioinformatic analysis tool to examine regional DNA methylation changes in embryonic stem cells (ESCs) during differentiation. The transcriptional silencing of pluripotency genes (PpGs) during ESC differentiation is accompanied by PpG enhancer (PpGe) silencing mediated by the demethylation of H3K4me1 by LSD1. Our MethylRAD data show that in the presence of LSD1 inhibitor, a significant fraction of LSD1-bound PpGe fails to gain DNA methylation. We further show that this effect is mostly observed in PpGes with low/intermediate CpG content. Underscoring the sensitivity and accuracy of MethylRAD sequencing, our study demonstrates that this method can detect small changes in DNA methylation in regulatory regions, including those with low/intermediate CpG content, thus asserting its use as a method of choice for diagnostic purposes. Full article
(This article belongs to the Special Issue Epigenetics in Stem Cells and Their Derivatives)
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Review

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17 pages, 2929 KiB  
Review
The Epigenetic Progenitor Origin of Cancer Reassessed: DNA Methylation Brings Balance to the Stem Force
by Marco Bruschi
Epigenomes 2020, 4(2), 8; https://doi.org/10.3390/epigenomes4020008 - 28 May 2020
Cited by 6 | Viewed by 4309
Abstract
Cancer initiation and progression toward malignant stages occur as the results of accumulating genetic alterations and epigenetic dysregulation. During the last decade, the development of next generation sequencing (NGS) technologies and the increasing pan-genomic knowledge have revolutionized how we consider the evolving epigenetic [...] Read more.
Cancer initiation and progression toward malignant stages occur as the results of accumulating genetic alterations and epigenetic dysregulation. During the last decade, the development of next generation sequencing (NGS) technologies and the increasing pan-genomic knowledge have revolutionized how we consider the evolving epigenetic landscapes during homeostasis and tumor progression. DNA methylation represents the best studied mark and is considered as a common mechanism of epigenetic regulation in normal homeostasis and cancer. A remarkable amount of work has recently started clarifying the central role played by DNA methylation dynamics on the maintenance of cell identity and on cell fate decisions during the different steps of normal development and tumor evolution. Importantly, a growing number of studies show that DNA methylation is key in the maintenance of adult stemness and in orchestrating commitment in multiple ways. Perturbations of the normal DNA methylation patterns impair the homeostatic balance and can lead to tumor initiation. Therefore, DNA methylation represents an interesting therapeutic target to recover homeostasis in tumor stem cells. Full article
(This article belongs to the Special Issue Epigenetics in Stem Cells and Their Derivatives)
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