Epigenetic Regulation of Stem Cell Fate Choice

Dear Colleagues,

Stem cell fate is regulated precisely and dynamically by a network of epigenetic signals. The epigenetic profile directly determines the developmental potential of stem cells, including pluripotency establishment, self-renewal, lineage-specific differentiation, as well as apoptosis and stem cell aging. On one hand, somatic cells can be reprogrammed into pluripotent status using a cocktail of transcriptional factors (e.g., Oct4, Sox2, Klf4, c-Myc) or a set of small molecules. On the other hand, to initiate the exit from pluripotency toward differentiation, cells need to disable pluripotency-specific epigenetic networks and activate lineage-specific pathways. In response to differentiation signals, stem cells dismantle the pluripotency network and shut down the expression of the stem cell core transcription factors. Additionally, embryonic stem cells (ESCs) can exist in naïve or primed states with distinct transcriptional regulatory networks, epigenotypes, and signaling requirements. Primed cells can be reverted to the pluripotent status by Klf4, c-Myc, or Nanog in the presence of LIF. Conversely, naive ES cells can be induced into the primed state by activating the FGF2/Activin pathway. Furthermore, ESCs can become homogeneous “ground-state” pluripotent stem cells under the influence of two small-molecule MEK/ERK and GSK inhibitors plus LIF (2i/LIF). Finally, the decline in stem cell function, often referred to as stem cell exhaustion, is a critical hallmark of ageing. However, specific epigenetic mechanisms involved in the inter-conversion of these states remain to be characterized.

This Special Issue will focus on the epigenetic mechanisms that determine stem cell fate, including in vitro and in vivo reprogramming, naïve-primed stage conversion, self-renewal, lineage differentiation, and stem cell aging. We welcome manuscripts (reviews, research, and technology tool articles) with a focus on the following areas:

• The regulatory role of epigenotypes (e.g., DNA and histone modifications) in stem cell fate transition and aging;
• Noncoding RNAs as critical epigenetic regulators;
• RNA modifications (m6A writers, erasers, and readers);
• Regulation of 3D chromatin structure;
• Controlling stem cell fate by small molecules;
• Epigenetics at the single cell level.

Dr. Jifan Hu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Epigenomes is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• stem cell fate
• epigenetics
• stem cell aging