Abstract
Genome editing technology has evolved rather quickly and become accessible to most researchers. It has resulted in far reaching implications and a number of novel designer systems including epigenome editing. Epigenome editing utilizes a combination of nuclease-null genome editing systems and effector domains to modulate gene expression. In particular, Zinc Finger, Transcription-Activator-Like Effector, and CRISPR/Cas9 have emerged as modular systems that can be modified to allow for precision manipulation of epigenetic marks without altering underlying DNA sequence. This review contains a comprehensive catalog of effector domains that can be used with components of genome editing systems to achieve epigenome editing. Ultimately, the evidence-based design of epigenome editing offers a novel improvement to the limited attenuation strategies. There is much potential for editing and/or correcting gene expression in somatic cells toward a new era of functional genomics and personalized medicine.
Highlights
The modulation of gene expression can be achieved by a variety of biotechnologies such as RNA interference, non-precision drugs, and artificial transcription factors (ATFs)
DCas9 The Clustered Regulatory Interspaced Short Palindromic Repeats (CRISPR)/CRISPR-Associated Protein 9 (Cas9) system has been used to alter transcription [79,80,81,82,83,84,85,86,87,88]. This has been achieved by targeting with synthetic guide RNA (sgRNA) and a catalytically inactivated Cas9, which creates a RNA-based targeting system that can be fused to effector domains
When comparing the ability to drive gene expression by targeting enhancers, it was found that Transcription-Activator-Like Effector (TALE) could outperform CRISPR/Cas9 and the authors recommended an approach combining both systems for highly efficient transcriptional regulation [54]
Summary
The modulation of gene expression can be achieved by a variety of biotechnologies such as RNA interference, non-precision drugs, and artificial transcription factors (ATFs). CRISPR/Cas9 has been used to remove CTCF binding sites in the Hox gene clusters during embryonic stem cell differentiation in cervical motor neurons and disrupt the topological chromatin boundaries, turning repressed chromatin into active chromatin by preventing CTCFs targeted function as a genomic insulator [47]. This modification for transcriptional alterations involves exclusion or inactivation of nuclease activity followed by use of the targeting system fused to a modular effector domain and is known as epigenome editing.
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