Table 2.

Recent Advances in CRISPR-based Epigenome Editing

Advancement	Reference
Epigenetic marks and chromatin states modulation (dCas9 nuclease-based fusions)
dCas9 (CRISPRi) (transcriptional interference)	[28]
dCas9-VP64 (transcriptional activation)	[29]
dCas9-VPR (VP64-p65-Rta) (transcriptional activation)	[56]
dCas9-KRAB (Krüppel associated box) (transcriptional repression)	[28]
dCas9-P300 (histone acetylation)	[8]
dCas9-LSD1 (histone demethylation)	[27]
dCas9-DNMT3A (DNA methylation)	[57]
dCas9-peptide repeat and scFv-TET1 catalytic domain fusions (DNA demethylation)	[30]
mRNA and protein localization tracking
RCas9 (nuclear-localized RNA-targeting dCas9) (mRNA tracking)	[31]
SLENDR (single-cell labeling of endogenous proteins by CRISPR/Cas9-mediated homology-directed repair) (protein tracking)	[32]
Multiplexed labeling of chromatin loci for tracking chromatin dynamic
CRISPR-Multicolor (multiple loci labeling)	[34]
CRISPRainbow (multiple loci labeling)	[35]
Reverse information flow from RNA to DNA
RT-Cas1(reverse transcriptase-Cas1) (reverse transcription)	[58]
Scarless genome editing
recCas9 (dCas9-serine recombinase) (genetic recombination)	[59]
Orthogonal gene knockout and transcriptional activation
SpCas9 with ‘dead RNAs’ (knock out and activate different genes in the same cell)	[60]