The Epigenome in Pluripotency and Differentiation

Abstract

The ability to culture pluripotent stem cells and direct their differentiation into specific cell types in vitro provides a valuable experimental system for modeling pluripotency, development and cellular differentiation. High-throughput profiling of the transcriptomes and epigenomes of pluripotent stem cells and their differentiated derivatives has led to identification of patterns characteristic of each cell type, discovery of new regulatory features in the epigenome and early insights into the complexity of dynamic interactions among regulatory elements. This work has also revealed potential limitations of the use of pluripotent stem cells as in vitro models of developmental events, due to epigenetic variability among different pluripotent stem cell lines and epigenetic instability during derivation and culture, particularly at imprinted and X-inactivated loci. This review focuses on the two most well-studied epigenetic mechanisms, DNA methylation and histone modifications, within the context of pluripotency and differentiation.

Keywords::

• differentiation
• DNA methylation
• epigenome
• histone modification
• imprinting
• pluripotency
• sequencing
• stem cells
• X inactivation

Acknowledgements

The authors would like to thank the National Institute of General Medical Sciences (NIGMS) for use of image 2562 from the NIGMS Image and Video Gallery (http://images.nigms.nih.gov/), which was the basis for Figure 1.

Financial & competing interests disclosure

RD Thiagarajan, R Morey and LC Laurent are supported by funds from the University of California, San Diego Department of Reproductive Medicine. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

RD Thiagarajan, R Morey and LC Laurent are supported by funds from the University of California, San Diego Department of Reproductive Medicine. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.