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Genetic and epigenetic control of gene expression by CRISPR–Cas systems

Lo, Albert, Qi, Lei·2017·F1000Research
DOI 10.12688/f1000research.11113.1PMC PMC5464239
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Abstract

The discovery and adaption of bacterial clustered regularly interspaced short palindromic repeats (CRISPR)–CRISPR-associated (Cas) systems has revolutionized the way researchers edit genomes. Engineering of catalytically inactivated Cas variants (nuclease-deficient or nuclease-deactivated [dCas]) combined with transcriptional repressors, activators, or epigenetic modifiers enable sequence-specific regulation of gene expression and chromatin state. These CRISPR–Cas-based technologies have contributed to the rapid development of disease models and functional genomics screening approaches, which can facilitate genetic target identification and drug discovery. In this short review, we will cover recent advances of CRISPR–dCas9 systems and their use for transcriptional repression and activation, epigenome editing, and engineered synthetic circuits for complex control of the mammalian genome.

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Figure 1. Clustered regularly interspaced short palindromic repeats (CRISPR)–CRISPR-associated 9 (Cas9) systems for genome editing and gene regulation. A. CRISPR–Cas9-mediated site-specific genome editing is accomplished by an RNA-guided DNA nuclease protein and a programmable single guide RNA (sgRNA). B. Nuclease-deficient Cas9 (dCas9) is engineered by introducing mutations (H841A and D10A) into catalytic residues of the HNH and RuvC nuclease domains. dCas9 therefore becomes a universal RNA-guided DNA-binding protein. C. Summary of CRISPR–Cas9-based genome engineering applications. D. Summary of CRISPR–dCas9-based genome engineering applications. PAM, protospacer-adjacent motif.
Figure 1. Clustered regularly interspaced short palindromic repeats (CRISPR)–CRISPR-associated 9 (Cas9) systems for genome editing and gene regulation. A. CRISPR–Cas9-mediated site-specific genome editing is accomplished by an RNA-guided DNA nuclease protein and a programmable single guide RNA (sgRNA). B. Nuclease-deficient Cas9 (dCas9) is engineered by introducing mutations (H841A and D10A) into catalytic residues of the HNH and RuvC nuclease domains. dCas9 therefore becomes a universal RNA-guided DNA-binding protein. C. Summary of CRISPR–Cas9-based genome engineering applications. D. Summary of CRISPR–dCas9-based genome engineering applications. PAM, protospacer-adjacent motif.CC BY · PubMed Central
Figure 2. Control of gene expression by clustered regularly interspaced short palindromic repeats (CRISPR)–nuclease-deficient CRISPR-associated 9 (dCas9) systems. A. CRISPR interference (CRISPRi) for gene repression. The CRISPR–Cas9 complex can interfere with the assembly of RNA polymerases (RNAPs) at the transcriptional initiation step or disrupt the elongation of RNAPs to abrogate gene expression. In addition, a transcriptional repressor such as Krüppel-associated box (KRAB) can be coupled with dCas9 to achieve gene repression. B. CRISPR activation (CRISPRa) for gene expression. dCas9 can be tethered with a transcriptional activator, for instance: 1) four copies of the herpes simplex viral protein 16 (VP16) activation domain (dCas9–VP64); 2) an aptamer-based recruitment system termed synergistic activation mediator (SAM), which uses combinatorial RNAs including single guide RNA (sgRNA) and MS2 RNA aptamers to recruit the MS2 bacteriophage coat protein (MCP) fused with p65 and heat shock factor 1 (HSF1); 3) a SunTag system that utilizes an array of small peptide epitopes to recruit multiple copies of single-chain variable fragment (scFv) fused with VP64; 4) a tandem fusion of three transcriptional activators including VP64, p65, and the Epstein–Barr virus R transactivator (RTa), or VPR, to augment gene expression. C. CRISPR–dCas9-based epigenome engineering. DNA and histone landmarks can be programmed in a designer manner by coupling dCas9 with specific epigenetic modifiers. For instance, fusing LSD1 demethylase with dCas9 can erase methylation of histone H3 lysine 4 (H3K4me2) near the enhancer region to abrogate gene expression, whereas the dCas9–p300 acetyltransferase chimeric protein increases acetylation of histone H3 lysine 27 (H3K27) at the enhancer and promoter to enhance gene expression. Alternatively, the DNA methylation status at the CpG-rich promoter can be modulated by a DNA methyltransferase (DNMT3a) or demethylase (TET1) to repress or augment gene expression, respectively.
Figure 2. Control of gene expression by clustered regularly interspaced short palindromic repeats (CRISPR)–nuclease-deficient CRISPR-associated 9 (dCas9) systems. A. CRISPR interference (CRISPRi) for gene repression. The CRISPR–Cas9 complex can interfere with the assembly of RNA polymerases (RNAPs) at the transcriptional initiation step or disrupt the elongation of RNAPs to abrogate gene expression. In addition, a transcriptional repressor such as Krüppel-associated box (KRAB) can be coupled with dCas9 to achieve gene repression. B. CRISPR activation (CRISPRa) for gene expression. dCas9 can be tethered with a transcriptional activator, for instance: 1) four copies of the herpes simplex viral protein 16 (VP16) activation domain (dCas9–VP64); 2) an aptamer-based recruitment system termed synergistic activation mediator (SAM), which uses combinatorial RNAs including single guide RNA (sgRNA) and MS2 RNA aptamers to recruit the MS2 bacteriophage coat protein (MCP) fused with p65 and heat shock factor 1 (HSF1); 3) a SunTag system that utilizes an array of small peptide epitopes to recruit multiple copies of single-chain variable fragment (scFv) fused with VP64; 4) a tandem fusion of three transcriptional activators including VP64, p65, and the Epstein–Barr virus R transactivator (RTa), or VPR, to augment gene expression. C. CRISPR–dCas9-based epigenome engineering. DNA and histone landmarks can be programmed in a designer manner by coupling dCas9 with specific epigenetic modifiers. For instance, fusing LSD1 demethylase with dCas9 can erase methylation of histone H3 lysine 4 (H3K4me2) near the enhancer region to abrogate gene expression, whereas the dCas9–p300 acetyltransferase chimeric protein increases acetylation of histone H3 lysine 27 (H3K27) at the enhancer and promoter to enhance gene expression. Alternatively, the DNA methylation status at the CpG-rich promoter can be modulated by a DNA methyltransferase (DNMT3a) or demethylase (TET1) to repress or augment gene expression, respectively.CC BY · PubMed Central
Figure 3. Synthetic approaches for complex and precise control of clustered regularly interspaced short palindromic repeats (CRISPR)–nuclease-deficient CRISPR-associated 9 (dCas9) systems. A. Control of CRISPR–dCas9 systems by light-inducible heterodimerization proteins. dCas9 and transcriptional effector (e.g. four copies of Herpes simplex viral protein 16 [VP64]) can be decoupled and fused to CRY and CIB, respectively. Upon sensing blue light, VP64 is recruited to dCas9 to activate gene expression. B. CRISPR–dCas9 systems can be rendered chemically controlled. Small-molecule-induced heterodimerization domains (e.g. FRB::FKBP, ABI::PYL1, and GAI::GID1) are introduced to dCas9–effector split systems for transcriptional controls. Binding of corresponding chemical (e.g. rapamycin, abscisic acid [ABA], or gibberellin [GA]) induces gene regulation by CRISPR–dCas9. C. Simultaneous gene activation and repression using a scaffold RNA (scRNA) system. A hybrid RNA consisting of an sgRNA and an RNA aptamer (e.g. MS2, com, PP7) is able to recruit the cognate RNA-binding protein (e.g. MCP, COM, PCP) tethered to either an activator (e.g. VP64) or a repressor (e.g. Krüppel-associated box [KRAB]). D. CRISPR–dCas9 systems can be regulated by protein destabilization domains. Structurally unstable protein domains such as estrogen receptor (ER) or the dihydrofolate reductase (DHFR) are fused to a chimeric protein consisting of an aptamer-binding protein (e.g. MCP or PCP) and a transcriptional activator (e.g. p65–HSF1 or VP64). These unfolded and destabilized domains increase fusion protein turnover by rapid proteasome-mediated degradation. Small molecules can bind and stabilize those domains (e.g. binding of 4OHT [4-hydroxytamoxifen] stabilizes ER, and binding of TMP [trimethoprim] stabilizes DHFR), allowing the control of gene expression. E. Control of CRISPR–dCas9 systems by RNA switchable devices. The single guide RNA (sgRNA) can be engineered to become a biosensor by fusing it with signal-responsive RNA aptamers. In the absence of certain signals, the guide region of the sgRNA pairs with the antisense stem and therefore cannot bind to its target DNA. Upon sensing specific signals by the RNA aptamers, a conformational change allows the guide region of the sgRNA to bring the dCas9 or dCas9–effector complex to the target DNA site, thereby altering gene expression.
Figure 3. Synthetic approaches for complex and precise control of clustered regularly interspaced short palindromic repeats (CRISPR)–nuclease-deficient CRISPR-associated 9 (dCas9) systems. A. Control of CRISPR–dCas9 systems by light-inducible heterodimerization proteins. dCas9 and transcriptional effector (e.g. four copies of Herpes simplex viral protein 16 [VP64]) can be decoupled and fused to CRY and CIB, respectively. Upon sensing blue light, VP64 is recruited to dCas9 to activate gene expression. B. CRISPR–dCas9 systems can be rendered chemically controlled. Small-molecule-induced heterodimerization domains (e.g. FRB::FKBP, ABI::PYL1, and GAI::GID1) are introduced to dCas9–effector split systems for transcriptional controls. Binding of corresponding chemical (e.g. rapamycin, abscisic acid [ABA], or gibberellin [GA]) induces gene regulation by CRISPR–dCas9. C. Simultaneous gene activation and repression using a scaffold RNA (scRNA) system. A hybrid RNA consisting of an sgRNA and an RNA aptamer (e.g. MS2, com, PP7) is able to recruit the cognate RNA-binding protein (e.g. MCP, COM, PCP) tethered to either an activator (e.g. VP64) or a repressor (e.g. Krüppel-associated box [KRAB]). D. CRISPR–dCas9 systems can be regulated by protein destabilization domains. Structurally unstable protein domains such as estrogen receptor (ER) or the dihydrofolate reductase (DHFR) are fused to a chimeric protein consisting of an aptamer-binding protein (e.g. MCP or PCP) and a transcriptional activator (e.g. p65–HSF1 or VP64). These unfolded and destabilized domains increase fusion protein turnover by rapid proteasome-mediated degradation. Small molecules can bind and stabilize those domains (e.g. binding of 4OHT [4-hydroxytamoxifen] stabilizes ER, and binding of TMP [trimethoprim] stabilizes DHFR), allowing the control of gene expression. E. Control of CRISPR–dCas9 systems by RNA switchable devices. The single guide RNA (sgRNA) can be engineered to become a biosensor by fusing it with signal-responsive RNA aptamers. In the absence of certain signals, the guide region of the sgRNA pairs with the antisense stem and therefore cannot bind to its target DNA. Upon sensing specific signals by the RNA aptamers, a conformational change allows the guide region of the sgRNA to bring the dCas9 or dCas9–effector complex to the target DNA site, thereby altering gene expression.CC BY · PubMed Central

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Metadata

Authors
Lo, A., & Qi, L.
ORCID
Qi, Lei
Venue
F1000Research
Publisher
F1000 Research Ltd
Published
2017-05-25
Volume
6
Pages
747
ISSN
2046-1402
DOI
10.12688/f1000research.11113.1
PMC
PMC5464239
Cited by
72
References
22
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)
Funders
  • Alfred P. Sloan Foundation
  • NIH Office of the Director (DP5 OD017887)
  • The Pew Charitable Trusts

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