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Article ; Online: Auxin-inducible degron 2 system deciphers functions of CTCF domains in transcriptional regulation.

Hyle, Judith / Djekidel, Mohamed Nadhir / Williams, Justin / Wright, Shaela / Shao, Ying / Xu, Beisi / Li, Chunliang

2023 Volume 24, Issue 1, Page(s) 14

Abstract: Background: CTCF is a well-established chromatin architectural protein that also plays various roles in transcriptional regulation. While CTCF biology has been extensively studied, how the domains of CTCF function to regulate transcription remains ... ...

Abstract	Background: CTCF is a well-established chromatin architectural protein that also plays various roles in transcriptional regulation. While CTCF biology has been extensively studied, how the domains of CTCF function to regulate transcription remains unknown. Additionally, the original auxin-inducible degron 1 (AID1) system has limitations in investigating the function of CTCF. Results: We employ an improved auxin-inducible degron technology, AID2, to facilitate the study of acute depletion of CTCF while overcoming the limitations of the previous AID system. As previously observed through the AID1 system and steady-state RNA analysis, the new AID2 system combined with SLAM-seq confirms that CTCF depletion leads to modest nascent and steady-state transcript changes. A CTCF domain sgRNA library screening identifies the zinc finger (ZF) domain as the region within CTCF with the most functional relevance, including ZFs 1 and 10. Removal of ZFs 1 and 10 reveals genomic regions that independently require these ZFs for DNA binding and transcriptional regulation. Notably, loci regulated by either ZF1 or ZF10 exhibit unique CTCF binding motifs specific to each ZF. Conclusions: By extensively comparing the AID1 and AID2 systems for CTCF degradation in SEM cells, we confirm that AID2 degradation is superior for achieving miniAID-tagged protein degradation without the limitations of the AID1 system. The model we create that combines AID2 depletion of CTCF with exogenous overexpression of CTCF mutants allows us to demonstrate how peripheral ZFs intricately orchestrate transcriptional regulation in a cellular context for the first time.
MeSH term(s)	CCCTC-Binding Factor/metabolism ; Indoleacetic Acids ; Gene Expression Regulation ; Zinc Fingers ; Genome
Chemical Substances	CCCTC-Binding Factor ; Indoleacetic Acids
Language	English
Publishing date	2023-01-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-022-02843-3
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Article ; Online: RNA-binding protein RBM5 plays an essential role in acute myeloid leukemia by activating the oncogenic protein HOXA9.

Zhang, Mengli / Hyle, Judith / Chen, Xiaowen / Xin, Ye / Jin, Yingcai / Zhang, Jianxiang / Yang, Xue / Chen, Xinfeng / Wright, Shaela / Liu, Zhenling / Rosikiewicz, Wojciech / Xu, Beisi / He, Liusheng / Liu, Hong / Ping, Nana / Wu, Depei / Wen, Feiqiu / Li, Chunliang / Xu, Peng

Genome biology

2024 Volume 25, Issue 1, Page(s) 16

Abstract: Background: The oncogenic protein HOXA9 plays a critical role in leukemia transformation and maintenance, and its aberrant expression is a hallmark of most aggressive acute leukemia. Although inhibiting the upstream regulators of HOXA9 has been proven ... ...

Abstract	Background: The oncogenic protein HOXA9 plays a critical role in leukemia transformation and maintenance, and its aberrant expression is a hallmark of most aggressive acute leukemia. Although inhibiting the upstream regulators of HOXA9 has been proven as a significant therapeutic intervention, the comprehensive regulation network controlling HOXA9 expression in leukemia has not been systematically investigated. Results: Here, we perform genome-wide CRISPR/Cas9 screening in the HOXA9-driven reporter acute leukemia cells. We identify a poorly characterized RNA-binding protein, RBM5, as the top candidate gene required to maintain leukemia cell fitness. RBM5 is highly overexpressed in acute myeloid leukemia (AML) patients compared to healthy individuals. RBM5 loss triggered by CRISPR knockout and shRNA knockdown significantly impairs leukemia maintenance in vitro and in vivo. Through domain CRISPR screening, we reveal that RBM5 functions through a noncanonical transcriptional regulation circuitry rather than RNA splicing, such an effect depending on DNA-binding domains. By integrative analysis and functional assays, we identify HOXA9 as the downstream target of RBM5. Ectopic expression of HOXA9 rescues impaired leukemia cell proliferation upon RBM5 loss. Importantly, acute protein degradation of RBM5 through auxin-inducible degron system immediately reduces HOXA9 transcription. Conclusions: We identify RBM5 as a new upstream regulator of HOXA9 and reveal its essential role in controlling the survival of AML. These functional and molecular mechanisms further support RBM5 as a promising therapeutic target for myeloid leukemia treatment.
MeSH term(s)	Humans ; Cell Cycle Proteins/metabolism ; Cell Proliferation ; DNA-Binding Proteins/metabolism ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Neoplasm Proteins/metabolism ; Oncogene Proteins/metabolism ; RNA-Binding Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Cell Cycle Proteins ; DNA-Binding Proteins ; Homeodomain Proteins ; Neoplasm Proteins ; Oncogene Proteins ; RBM5 protein, human ; RNA-Binding Proteins ; Tumor Suppressor Proteins ; homeobox protein HOXA9
Language	English
Publishing date	2024-01-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-023-03149-8
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Article ; Online: Systematic characterization of the HOXA9 downstream targets in MLL-r leukemia by noncoding CRISPR screens.

Wright, Shaela / Zhao, Xujie / Rosikiewicz, Wojciech / Mryncza, Shelby / Hyle, Judith / Qi, Wenjie / Liu, Zhenling / Yi, Siqi / Cheng, Yong / Xu, Beisi / Li, Chunliang

Nature communications

2023 Volume 14, Issue 1, Page(s) 7464

Abstract: Accumulating evidence indicates that HOXA9 dysregulation is necessary and sufficient for leukemic transformation and maintenance. However, it remains largely unknown how HOXA9, as a homeobox transcriptional factor, binds to noncoding regulatory sequences ...

Abstract	Accumulating evidence indicates that HOXA9 dysregulation is necessary and sufficient for leukemic transformation and maintenance. However, it remains largely unknown how HOXA9, as a homeobox transcriptional factor, binds to noncoding regulatory sequences and controls the downstream genes. Here, we conduct dropout CRISPR screens against 229 HOXA9-bound peaks identified by ChIP-seq. Integrative data analysis identifies reproducible noncoding hits, including those located in the distal enhancer of FLT3 and intron of CDK6. The Cas9-editing and dCas9-KRAB silencing of the HOXA9-bound sites significantly reduce corresponding gene transcription and impair cell proliferation in vitro, and in vivo by transplantation into NSG female mice. In addition, RNA-seq, Q-PCR analysis, chromatin accessibility change, and chromatin conformation evaluation uncover the noncoding regulation mechanism of HOXA9 and its functional downstream genes. In summary, our work improves our understanding of how HOXA9-associated transcription programs reconstruct the regulatory network specifying MLL-r dependency.
MeSH term(s)	Female ; Mice ; Animals ; Homeodomain Proteins/metabolism ; Transcription Factors/metabolism ; Leukemia/genetics ; Neoplasm Proteins/metabolism ; Up-Regulation ; Chromatin ; Gene Expression Regulation, Leukemic
Chemical Substances	Homeodomain Proteins ; Transcription Factors ; Neoplasm Proteins ; Chromatin
Language	English
Publishing date	2023-11-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-43264-5
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Article ; Online: Interrogating bromodomain inhibitor resistance in KMT2A-rearranged leukemia through combinatorial CRISPR screens.

Wright, Shaela / Hu, Jianzhong / Wang, Hong / Hyle, Judith / Zhang, Yang / Du, Guoqing / Konopleva, Marina Y / Kornblau, Steven M / Djekidel, Mohamed Nadhir / Rosikiewicz, Wojciech / Xu, Beisi / Lu, Rui / Yang, Jun J / Li, Chunliang

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 16, Page(s) e2220134120

Abstract: Bromo- and extra-terminal domain inhibitors (BETi) have exhibited therapeutic activities in many cancers. However, the mechanisms controlling BETi response and resistance are not well understood. We conducted genome-wide loss-of-function CRISPR screens ... ...

Abstract	Bromo- and extra-terminal domain inhibitors (BETi) have exhibited therapeutic activities in many cancers. However, the mechanisms controlling BETi response and resistance are not well understood. We conducted genome-wide loss-of-function CRISPR screens using BETi-treated KMT2A-rearranged (KMT2A-r) cell lines. We revealed that
MeSH term(s)	Humans ; Clustered Regularly Interspaced Short Palindromic Repeats ; Glycogen Synthase Kinase 3/metabolism ; Cell Line, Tumor ; Leukemia/drug therapy ; Leukemia/genetics ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Repressor Proteins/metabolism
Chemical Substances	Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; SPOP protein, human ; Nuclear Proteins ; Repressor Proteins
Language	English
Publishing date	2023-04-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2220134120
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Article ; Online: A

Zhang, Yang / Hyle, Judith / Wright, Shaela / Shao, Ying / Zhao, Xujie / Zhang, Hui / Li, Chunliang

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 52, Page(s) 26644–26652

Abstract: Loss of function ... ...

Abstract	Loss of function of
Language	English
Publishing date	2019-12-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1909720116
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Article ; Online: Acute depletion of CTCF directly affects MYC regulation through loss of enhancer-promoter looping.

Hyle, Judith / Zhang, Yang / Wright, Shaela / Xu, Beisi / Shao, Ying / Easton, John / Tian, Liqing / Feng, Ruopeng / Xu, Peng / Li, Chunliang

Nucleic acids research

2019 Volume 47, Issue 13, Page(s) 6699–6713

Abstract: Numerous pieces of evidence support the complex, 3D spatial organization of the genome dictates gene expression. CTCF is essential to define topologically associated domain boundaries and to facilitate the formation of insulated chromatin loop structures. ...

Abstract	Numerous pieces of evidence support the complex, 3D spatial organization of the genome dictates gene expression. CTCF is essential to define topologically associated domain boundaries and to facilitate the formation of insulated chromatin loop structures. To understand CTCF's direct role in global transcriptional regulation, we integrated the miniAID-mClover3 cassette to the endogenous CTCF locus in a human pediatric B-ALL cell line, SEM, and an immortal erythroid precursor cell line, HUDEP-2, to allow for acute depletion of CTCF protein by the auxin-inducible degron system. In SEM cells, CTCF loss notably disrupted intra-TAD loops and TAD integrity in concurrence with a reduction in CTCF-binding affinity, while showing no perturbation to nuclear compartment integrity. Strikingly, the overall effect of CTCF's loss on transcription was minimal. Whole transcriptome analysis showed hundreds of genes differentially expressed in CTCF-depleted cells, among which MYC and a number of MYC target genes were specifically downregulated. Mechanically, acute depletion of CTCF disrupted the direct interaction between the MYC promoter and its distal enhancer cluster residing ∼1.8 Mb downstream. Notably, MYC expression was not profoundly affected upon CTCF loss in HUDEP-2 cells suggesting that CTCF could play a B-ALL cell line specific role in maintaining MYC expression.
MeSH term(s)	CCCTC-Binding Factor/deficiency ; CCCTC-Binding Factor/physiology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Nucleus/ultrastructure ; Chromatin/genetics ; Chromatin/ultrastructure ; Down-Regulation ; Enhancer Elements, Genetic/genetics ; Erythroid Precursor Cells/metabolism ; Gene Expression Regulation, Leukemic ; Gene Knock-In Techniques ; Genes, Reporter ; Genes, myc ; Humans ; Nucleic Acid Conformation ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-myc/biosynthesis ; Transcriptome
Chemical Substances	CCCTC-Binding Factor ; CTCF protein, human ; Chromatin ; MYC protein, human ; Proto-Oncogene Proteins c-myc
Language	English
Publishing date	2019-05-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkz462
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Article ; Online: Acute depletion of CTCF rewires genome-wide chromatin accessibility.

Xu, Beisi / Wang, Hong / Wright, Shaela / Hyle, Judith / Zhang, Yang / Shao, Ying / Niu, Mingming / Fan, Yiping / Rosikiewicz, Wojciech / Djekidel, Mohamed Nadhir / Peng, Junmin / Lu, Rui / Li, Chunliang

Genome biology

2021 Volume 22, Issue 1, Page(s) 244

Abstract: Background: The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of ... ...

Abstract	Background: The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of CTCF globally reduces chromatin interactions but does not significantly alter transcription. Results: Here, we systematically integrate multi-omics data including ATAC-seq, RNA-seq, WGBS, Hi-C, Cut&Run, and CRISPR-Cas9 survival dropout screens, and time-solved deep proteomic and phosphoproteomic analyses in cells carrying auxin-induced degron at endogenous CTCF locus. Acute CTCF protein degradation markedly rewires genome-wide chromatin accessibility. Increased accessible chromatin regions are frequently located adjacent to CTCF-binding sites at promoter regions and insulator sites associated with enhanced transcription of nearby genes. In addition, we use CTCF-associated multi-omics data to establish a combinatorial data analysis pipeline to discover CTCF co-regulatory partners. We successfully identify 40 candidates, including multiple established partners. Interestingly, many CTCF co-regulators that have alterations of their respective downstream gene expression do not show changes of their own expression levels across the multi-omics measurements upon acute CTCF loss, highlighting the strength of our system to discover hidden co-regulatory partners associated with CTCF-mediated transcription. Conclusions: This study highlights that CTCF loss rewires genome-wide chromatin accessibility, which plays a critical role in transcriptional regulation.
MeSH term(s)	Base Sequence ; Binding Sites ; CCCTC-Binding Factor/deficiency ; CCCTC-Binding Factor/metabolism ; Cell Line, Tumor ; Chromatin/metabolism ; Gene Deletion ; Gene Expression Regulation ; Genome, Human ; Genomics ; Humans ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Reproducibility of Results
Chemical Substances	BLCAP protein, human ; CCCTC-Binding Factor ; Chromatin ; Neoplasm Proteins
Language	English
Publishing date	2021-08-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-021-02466-0
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Article: Acute depletion of CTCF rewires genome-wide chromatin accessibility

Genome biology. 2021 Dec., v. 22, no. 1

2021

Abstract: BACKGROUND: The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of ... ...

Abstract	BACKGROUND: The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of CTCF globally reduces chromatin interactions but does not significantly alter transcription. RESULTS: Here, we systematically integrate multi-omics data including ATAC-seq, RNA-seq, WGBS, Hi-C, Cut&Run, and CRISPR-Cas9 survival dropout screens, and time-solved deep proteomic and phosphoproteomic analyses in cells carrying auxin-induced degron at endogenous CTCF locus. Acute CTCF protein degradation markedly rewires genome-wide chromatin accessibility. Increased accessible chromatin regions are frequently located adjacent to CTCF-binding sites at promoter regions and insulator sites associated with enhanced transcription of nearby genes. In addition, we use CTCF-associated multi-omics data to establish a combinatorial data analysis pipeline to discover CTCF co-regulatory partners. We successfully identify 40 candidates, including multiple established partners. Interestingly, many CTCF co-regulators that have alterations of their respective downstream gene expression do not show changes of their own expression levels across the multi-omics measurements upon acute CTCF loss, highlighting the strength of our system to discover hidden co-regulatory partners associated with CTCF-mediated transcription. CONCLUSIONS: This study highlights that CTCF loss rewires genome-wide chromatin accessibility, which plays a critical role in transcriptional regulation.
Keywords	CRISPR-Cas systems ; chromatin ; gene expression ; loci ; multiomics ; protein degradation ; proteomics ; sequence analysis ; transcription (genetics) ; transcription factors
Language	English
Dates of publication	2021-12
Size	p. 244.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-021-02466-0
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Foxp3 enhancers synergize to maximize regulatory T cell suppressive capacity.

Zong, Xinying / Hao, Xiaolei / Xu, Beisi / Crawford, Jeremy Chase / Wright, Shaela / Li, Jun / Zhang, Yang / Bai, Lu / He, Minghong / Jiang, Menglin / Fan, Yiping / Connelly, Jon P / Pruett-Miller, Shondra M / Berns, Hartmut / Janke, Laura / Li, Chunliang / Feng, Yongqiang

The Journal of experimental medicine

2021 Volume 218, Issue 8

Abstract: T reg cells bearing a diverse antigen receptor repertoire suppress pathogenic T cells and maintain immune homeostasis during their long lifespan. How their robust function is determined genetically remains elusive. Here, we investigate the regulatory ... ...

Abstract	T reg cells bearing a diverse antigen receptor repertoire suppress pathogenic T cells and maintain immune homeostasis during their long lifespan. How their robust function is determined genetically remains elusive. Here, we investigate the regulatory space of the cis-regulatory elements of T reg lineage-specifying factor Foxp3. Foxp3 enhancers are known as distinct readers of environmental cues controlling T reg cell induction or lineage stability. However, their single deficiencies cause mild, if any, immune dysregulation, leaving the key transcriptional mechanisms determining Foxp3 expression and thereby T reg cell suppressive capacity uncertain. We examined the collective activities of Foxp3 enhancers and found that they coordinate to maximize T reg cell induction, Foxp3 expression level, or lineage stability through distinct modes and that ablation of synergistic enhancers leads to lethal autoimmunity in young mice. Thus, the induction and maintenance of a diverse, stable T reg cell repertoire rely on combinatorial Foxp3 enhancers, suggesting broad, stage-specific, synergistic activities of cell-intrinsic factors and cell-extrinsic cues in determining T reg cell suppressive capacity.
MeSH term(s)	Animals ; Autoimmunity ; CRISPR-Cas Systems/genetics ; Cell Lineage ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic ; Epistasis, Genetic ; Female ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Lymphocyte Activation/immunology ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Antigen, T-Cell/metabolism ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/immunology ; Mice
Chemical Substances	Forkhead Transcription Factors ; Foxp3 protein, mouse ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2021-06-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20202415
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Article ; Online: Functional interrogation of HOXA9 regulome in MLLr leukemia via reporter-based CRISPR/Cas9 screen.

Zhang, Hao / Zhang, Yang / Zhou, Xinyue / Wright, Shaela / Hyle, Judith / Zhao, Lianzhong / An, Jie / Zhao, Xujie / Shao, Ying / Xu, Beisi / Lee, Hyeong-Min / Chen, Taosheng / Zhou, Yang / Chen, Xiang / Lu, Rui / Li, Chunliang

eLife

2020 Volume 9

Abstract: ... ...

Abstract	Aberrant
MeSH term(s)	Alleles ; CRISPR-Cas Systems ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; Epigenesis, Genetic ; Gene Expression Regulation, Leukemic ; Genes, Reporter ; Histone-Lysine N-Methyltransferase/genetics ; Homeodomain Proteins/metabolism ; Humans ; Leukemia/metabolism ; Myeloid-Lymphoid Leukemia Protein/genetics ; Upstream Stimulatory Factors/metabolism
Chemical Substances	Homeodomain Proteins ; KMT2A protein, human ; USF1 protein, human ; USF2 protein, human ; Upstream Stimulatory Factors ; homeobox protein HOXA9 ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
Language	English
Publishing date	2020-10-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.57858
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