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Article: Prioritisation of Candidate Genes Underpinning COVID-19 Host Genetic Traits Based on High-Resolution 3D Chromosomal Topology.

Thiecke, Michiel J / Yang, Emma J / Burren, Oliver S / Ray-Jones, Helen / Spivakov, Mikhail

2021 Volume 12, Page(s) 745672

Abstract: Genetic variants showing associations with specific biological traits and diseases detected by genome-wide association studies (GWAS) commonly map to non-coding DNA regulatory regions. Many of these regions are located considerable distances away from ... ...

Abstract	Genetic variants showing associations with specific biological traits and diseases detected by genome-wide association studies (GWAS) commonly map to non-coding DNA regulatory regions. Many of these regions are located considerable distances away from the genes they regulate and come into their proximity through 3D chromosomal interactions. We previously developed COGS, a statistical pipeline for linking GWAS variants with their putative target genes based on 3D chromosomal interaction data arising from high-resolution assays such as Promoter Capture Hi-C (PCHi-C). Here, we applied COGS to COVID-19 Host Genetic Consortium (HGI) GWAS meta-analysis data on COVID-19 susceptibility and severity using our previously generated PCHi-C results in 17 human primary cell types and SARS-CoV-2-infected lung carcinoma cells. We prioritise 251 genes putatively associated with these traits, including 16 out of 47 genes highlighted by the GWAS meta-analysis authors. The prioritised genes are expressed in a broad array of tissues, including, but not limited to, blood and brain cells, and are enriched for genes involved in the inflammatory response to viral infection. Our prioritised genes and pathways, in conjunction with results from other prioritisation approaches and targeted validation experiments, will aid in the understanding of COVID-19 pathology, paving the way for novel treatments.
Language	English
Publishing date	2021-10-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2021.745672
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Article ; Online: Cohesin-Dependent and -Independent Mechanisms Mediate Chromosomal Contacts between Promoters and Enhancers.

Thiecke, Michiel J / Wutz, Gordana / Muhar, Matthias / Tang, Wen / Bevan, Stephen / Malysheva, Valeriya / Stocsits, Roman / Neumann, Tobias / Zuber, Johannes / Fraser, Peter / Schoenfelder, Stefan / Peters, Jan-Michael / Spivakov, Mikhail

Cell reports

2020 Volume 32, Issue 3, Page(s) 107929

Abstract: It is currently assumed that 3D chromosomal organization plays a central role in transcriptional control. However, depletion of cohesin and CTCF affects the steady-state levels of only a minority of transcripts. Here, we use high-resolution Capture Hi-C ... ...

Abstract	It is currently assumed that 3D chromosomal organization plays a central role in transcriptional control. However, depletion of cohesin and CTCF affects the steady-state levels of only a minority of transcripts. Here, we use high-resolution Capture Hi-C to interrogate the dynamics of chromosomal contacts of all annotated human gene promoters upon degradation of cohesin and CTCF. We show that a majority of promoter-anchored contacts are lost in these conditions, but many contacts with distinct properties are maintained, and some new ones are gained. The rewiring of contacts between promoters and active enhancers upon cohesin degradation associates with rapid changes in target gene transcription as detected by SLAM sequencing (SLAM-seq). These results provide a mechanistic explanation for the limited, but consistent, effects of cohesin and CTCF depletion on steady-state transcription and suggest the existence of both cohesin-dependent and -independent mechanisms of enhancer-promoter pairing.
MeSH term(s)	Cell Cycle Proteins/metabolism ; Chromatin ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosomes/metabolism ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic/genetics ; Gene Expression Regulation ; HeLa Cells ; Humans ; Promoter Regions, Genetic ; Transcription, Genetic ; Cohesins
Chemical Substances	Cell Cycle Proteins ; Chromatin ; Chromosomal Proteins, Non-Histone ; DNA-Binding Proteins
Language	English
Publishing date	2020-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.107929
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Article ; Online: Vanishing white matter: deregulated integrated stress response as therapy target.

Abbink, Truus E M / Wisse, Lisanne E / Jaku, Ermelinda / Thiecke, Michiel J / Voltolini-González, Daniel / Fritsen, Hein / Bobeldijk, Sander / Ter Braak, Timo J / Polder, Emiel / Postma, Nienke L / Bugiani, Marianna / Struijs, Eduard A / Verheijen, Mark / Straat, Nina / van der Sluis, Sophie / Thomas, Adri A M / Molenaar, Douwe / van der Knaap, Marjo S

Annals of clinical and translational neurology

2019 Volume 6, Issue 8, Page(s) 1407–1422

Abstract: Objective: Vanishing white matter (VWM) is a fatal, stress-sensitive leukodystrophy that mainly affects children and is currently without treatment. VWM is caused by recessive mutations in eukaryotic initiation factor 2B (eIF2B) that is crucial for ... ...

Abstract	Objective: Vanishing white matter (VWM) is a fatal, stress-sensitive leukodystrophy that mainly affects children and is currently without treatment. VWM is caused by recessive mutations in eukaryotic initiation factor 2B (eIF2B) that is crucial for initiation of mRNA translation and its regulation during the integrated stress response (ISR). Mutations reduce eIF2B activity. VWM pathomechanisms remain unclear. In contrast with the housekeeping function of eIF2B, astrocytes are selectively affected in VWM. One study objective was to test our hypothesis that in the brain translation of specific mRNAs is altered by eIF2B mutations, impacting primarily astrocytes. The second objective was to investigate whether modulation of eIF2B activity could ameliorate this altered translation and improve the disease. Methods: Mice with biallelic missense mutations in eIF2B that recapitulate human VWM were used to screen for mRNAs with altered translation in brain using polysomal profiling. Findings were verified in brain tissue from VWM patients using qPCR and immunohistochemistry. The compound ISRIB (for "ISR inhibitor") was administered to VWM mice to increase eIF2B activity. Its effect on translation, neuropathology, and clinical signs was assessed. Results: In brains of VWM compared to wild-type mice we observed the most prominent changes in translation concerning ISR mRNAs; their expression levels correlated with disease severity. We substantiated these findings in VWM patients' brains. ISRIB normalized expression of mRNA markers, ameliorated brain white matter pathology and improved motor skills in VWM mice. Interpretation: The present findings show that ISR deregulation is central in VWM pathomechanisms and a viable target for therapy.
MeSH term(s)	Acetamides/pharmacology ; Activating Transcription Factor 4/metabolism ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Astrocytes/metabolism ; Brain/metabolism ; Cell Cycle Proteins/metabolism ; Cerebellum/drug effects ; Corpus Callosum/drug effects ; Cyclohexylamines/pharmacology ; Eukaryotic Initiation Factor-2B/genetics ; Eukaryotic Initiation Factor-2B/metabolism ; Humans ; Leukoencephalopathies/drug therapy ; Leukoencephalopathies/genetics ; Leukoencephalopathies/pathology ; Mice ; Mutation ; Protein Biosynthesis ; Protein-Serine-Threonine Kinases/metabolism ; White Matter/pathology
Chemical Substances	2-(4-chlorophenoxy)-N-(4-(2-(4-chlorophenoxy)acetamido)cyclohexyl)acetamide ; Acetamides ; Adaptor Proteins, Signal Transducing ; Atf4 protein, mouse ; Cell Cycle Proteins ; Cyclohexylamines ; EIF4EBP1 protein, human ; Eif4ebp1 protein, mouse ; Eukaryotic Initiation Factor-2B ; Activating Transcription Factor 4 (145891-90-3) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; eIF2alpha kinase, mouse (EC 2.7.11.1)
Language	English
Publishing date	2019-07-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2740696-9
ISSN	2328-9503 ; 2328-9503
ISSN (online)	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.50826
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Article ; Online: TOP1 inhibition therapy protects against SARS-CoV-2-induced lethal inflammation.

Ho, Jessica Sook Yuin / Mok, Bobo Wing-Yee / Campisi, Laura / Jordan, Tristan / Yildiz, Soner / Parameswaran, Sreeja / Wayman, Joseph A / Gaudreault, Natasha N / Meekins, David A / Indran, Sabarish V / Morozov, Igor / Trujillo, Jessie D / Fstkchyan, Yesai S / Rathnasinghe, Raveen / Zhu, Zeyu / Zheng, Simin / Zhao, Nan / White, Kris / Ray-Jones, Helen /

Malysheva, Valeriya / Thiecke, Michiel J / Lau, Siu-Ying / Liu, Honglian / Zhang, Anna Junxia / Lee, Andrew Chak-Yiu / Liu, Wen-Chun / Jangra, Sonia / Escalera, Alba / Aydillo, Teresa / Melo, Betsaida Salom / Guccione, Ernesto / Sebra, Robert / Shum, Elaine / Bakker, Jan / Kaufman, David A / Moreira, Andre L / Carossino, Mariano / Balasuriya, Udeni B R / Byun, Minji / Albrecht, Randy A / Schotsaert, Michael / Garcia-Sastre, Adolfo / Chanda, Sumit K / Miraldi, Emily R / Jeyasekharan, Anand D / TenOever, Benjamin R / Spivakov, Mikhail / Weirauch, Matthew T / Heinz, Sven / Chen, Honglin / Benner, Christopher / Richt, Juergen A / Marazzi, Ivan

Cell

2021 Volume 184, Issue 10, Page(s) 2618–2632.e17

Abstract: The ongoing pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory ... ...

Abstract	The ongoing pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Here, using multidimensional epigenetic, transcriptional, in vitro, and in vivo analyses, we report that topoisomerase 1 (TOP1) inhibition suppresses lethal inflammation induced by SARS-CoV-2. Therapeutic treatment with two doses of topotecan (TPT), an FDA-approved TOP1 inhibitor, suppresses infection-induced inflammation in hamsters. TPT treatment as late as 4 days post-infection reduces morbidity and rescues mortality in a transgenic mouse model. These results support the potential of TOP1 inhibition as an effective host-directed therapy against severe SARS-CoV-2 infection. TPT and its derivatives are inexpensive clinical-grade inhibitors available in most countries. Clinical trials are needed to evaluate the efficacy of repurposing TOP1 inhibitors for severe coronavirus disease 2019 (COVID-19) in humans.
MeSH term(s)	Animals ; COVID-19/enzymology ; COVID-19/pathology ; Chlorocebus aethiops ; DNA Topoisomerases, Type I/metabolism ; Humans ; Inflammation/drug therapy ; Inflammation/enzymology ; Inflammation/pathology ; Inflammation/virology ; Mesocricetus ; Mice ; Mice, Transgenic ; SARS-CoV-2/metabolism ; THP-1 Cells ; Topoisomerase I Inhibitors/pharmacology ; Topotecan/pharmacology ; Vero Cells ; COVID-19 Drug Treatment
Chemical Substances	Topoisomerase I Inhibitors ; Topotecan (7M7YKX2N15) ; DNA Topoisomerases, Type I (EC 5.99.1.2) ; TOP1 protein, human (EC 5.99.1.2)
Language	English
Publishing date	2021-03-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2021.03.051
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Article: Topoisomerase 1 inhibition therapy protects against SARS-CoV-2-induced inflammation and death in animal models.

Yuin Ho, Jessica Sook / Wing-Yee Mok, Bobo / Campisi, Laura / Jordan, Tristan / Yildiz, Soner / Parameswaran, Sreeja / Wayman, Joseph A / Gaudreault, Natasha N / Meekins, David A / Indran, Sabarish V / Morozov, Igor / Trujillo, Jessie D / Fstkchyan, Yesai S / Rathnasinghe, Raveen / Zhu, Zeyu / Zheng, Simin / Zhao, Nan / White, Kris / Ray-Jones, Helen /

Malysheva, Valeriya / Thiecke, Michiel J / Lau, Siu-Ying / Liu, Honglian / Junxia Zhang, Anna / Chak-Yiu Lee, Andrew / Liu, Wen-Chun / Aydillo, Teresa / Salom Melo, Betsaida / Guccione, Ernesto / Sebra, Robert / Shum, Elaine / Bakker, Jan / Kaufman, David A / Moreira, Andre L / Carossino, Mariano / Balasuriya, Udeni B R / Byun, Minji / Miraldi, Emily R / Albrecht, Randy A / Schotsaert, Michael / Garcia-Sastre, Adolfo / Chanda, Sumit K / Jeyasekharan, Anand D / TenOever, Benjamin R / Spivakov, Mikhail / Weirauch, Matthew T / Heinz, Sven / Chen, Honglin / Benner, Christopher / Richt, Juergen A / Marazzi, Ivan

bioRxiv : the preprint server for biology

2020

Abstract: The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory ... ...

Abstract	The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Here, using multidimensional epigenetic, transcriptional,
Language	English
Publishing date	2020-12-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.12.01.404483
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Article ; Online: Lineage-Specific Genome Architecture Links Enhancers and Non-coding Disease Variants to Target Gene Promoters.

Javierre, Biola M / Burren, Oliver S / Wilder, Steven P / Kreuzhuber, Roman / Hill, Steven M / Sewitz, Sven / Cairns, Jonathan / Wingett, Steven W / Várnai, Csilla / Thiecke, Michiel J / Burden, Frances / Farrow, Samantha / Cutler, Antony J / Rehnström, Karola / Downes, Kate / Grassi, Luigi / Kostadima, Myrto / Freire-Pritchett, Paula / Wang, Fan /

Stunnenberg, Hendrik G / Todd, John A / Zerbino, Daniel R / Stegle, Oliver / Ouwehand, Willem H / Frontini, Mattia / Wallace, Chris / Spivakov, Mikhail / Fraser, Peter

Cell

2016 Volume 167, Issue 5, Page(s) 1369–1384.e19

Abstract: Long-range interactions between regulatory elements and gene promoters play key roles in transcriptional regulation. The vast majority of interactions are uncharted, constituting a major missing link in understanding genome control. Here, we use promoter ...

Abstract	Long-range interactions between regulatory elements and gene promoters play key roles in transcriptional regulation. The vast majority of interactions are uncharted, constituting a major missing link in understanding genome control. Here, we use promoter capture Hi-C to identify interacting regions of 31,253 promoters in 17 human primary hematopoietic cell types. We show that promoter interactions are highly cell type specific and enriched for links between active promoters and epigenetically marked enhancers. Promoter interactomes reflect lineage relationships of the hematopoietic tree, consistent with dynamic remodeling of nuclear architecture during differentiation. Interacting regions are enriched in genetic variants linked with altered expression of genes they contact, highlighting their functional role. We exploit this rich resource to connect non-coding disease variants to putative target promoters, prioritizing thousands of disease-candidate genes and implicating disease pathways. Our results demonstrate the power of primary cell promoter interactomes to reveal insights into genomic regulatory mechanisms underlying common diseases.
MeSH term(s)	Blood Cells/cytology ; Cell Lineage ; Cell Separation ; Chromatin ; Disease/genetics ; Enhancer Elements, Genetic ; Epigenomics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Hematopoiesis ; Humans ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Quantitative Trait Loci
Chemical Substances	Chromatin
Language	English
Publishing date	2016-08-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2016.09.037
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Article ; Online: Topoisomerase 1 inhibition therapy protects against SARS-CoV-2-induced inflammation and death in animal models.

Malysheva, Valeriya / Thiecke, Michiel J / Lau, Siu-Ying / Liu, Honglian / Zhang, Anna Junxia / Lee, Andrew Chak-Yiu / Liu, Wen-Chun / Aydillo, Teresa / Melo, Betsaida S / Guccione, Ernesto / Sebra, Robert / Shum, Elaine / Bakker, Jan / Kaufman, David A / Moreira, Andre / Carossino, Mariano / Balasuriya, Udeni B R / Byun, Minji / Miraldi, Emily R / Albrecht, Randy A / Schotsaert, Michael / Garcia-Sastre, Adolfo / Chanda, Sumit K / Jeyasekharan, Anand D / TenOever, Benjamin R / Spivakov, Mikhail / Weirauch, Matthew T / Heinz, Sven / Chen, Honglin / Benner, Christopher / Richt, Juergen A / Marazzi, Ivan

bioRxiv

Abstract	The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Here, using multidimensional epigenetic, transcriptional, in vitro and in vivo analyses, we report that Topoisomerase 1 (Top1) inhibition suppresses lethal inflammation induced by SARS-CoV-2. Therapeutic treatment with two doses of Topotecan (TPT), a FDA-approved Top1 inhibitor, suppresses infection-induced inflammation in hamsters. TPT treatment as late as four days post-infection reduces morbidity and rescues mortality in a transgenic mouse model. These results support the potential of Top1 inhibition as an effective host-directed therapy against severe SARS-CoV-2 infection. TPT and its derivatives are inexpensive clinical-grade inhibitors available in most countries. Clinical trials are needed to evaluate the efficacy of repurposing Top1 inhibitors for COVID-19 in humans.
Keywords	covid19
Language	English
Publishing date	2020-12-01
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2020.12.01.404483
Database	COVID19

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Article: Lineage-Specific Genome Architecture Links Enhancers and Non-coding Disease Variants to Target Gene Promoters

Javierre, Biola M / Oliver S. Burren / Steven P. Wilder / Roman Kreuzhuber / Steven M. Hill / Sven Sewitz / Jonathan Cairns / Steven W. Wingett / Csilla VÃ¡rnai / Michiel J. Thiecke / Frances Burden / Samantha Farrow / Antony J. Cutler / Karola RehnstrÃ¶m / Kate Downes / Luigi Grassi / Myrto Kostadima / Paula Freire-Pritchett / Fan Wang /

Hendrik G. Stunnenberg / John A. Todd / Daniel R. Zerbino / Oliver Stegle / Willem H. Ouwehand / Mattia Frontini / Chris Wallace / Mikhail Spivakov / Peter Fraser

Cell. 2016 Nov. 17, v. 167

2016

Abstract	Long-range interactions between regulatory elements and gene promoters play key roles in transcriptional regulation. The vast majority of interactions are uncharted, constituting a major missing link in understanding genome control. Here, we use promoter capture Hi-C to identify interacting regions of 31,253 promoters in 17 human primary hematopoietic cell types. We show that promoter interactions are highly cell type specific and enriched for links between active promoters and epigenetically marked enhancers. Promoter interactomes reflect lineage relationships of the hematopoietic tree, consistent with dynamic remodeling of nuclear architecture during differentiation. Interacting regions are enriched in genetic variants linked with altered expression of genes they contact, highlighting their functional role. We exploit this rich resource to connect non-coding disease variants to putative target promoters, prioritizing thousands of disease-candidate genes and implicating disease pathways. Our results demonstrate the power of primary cell promoter interactomes to reveal insights into genomic regulatory mechanisms underlying common diseases.
Keywords	gene expression ; genes ; genetic variation ; humans ; regulatory sequences ; transcription (genetics) ; trees
Language	English
Dates of publication	2016-1117
Size	p. 1369-1384.e19.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2016.09.037
Database	NAL-Catalogue (AGRICOLA)

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Article: Prioritisation of Candidate Genes Underpinning COVID-19 Host Genetic Traits Based on High-Resolution 3D Chromosomal Topology.

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Article ; Online: Cohesin-Dependent and -Independent Mechanisms Mediate Chromosomal Contacts between Promoters and Enhancers.

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Article ; Online: Vanishing white matter: deregulated integrated stress response as therapy target.

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Article ; Online: TOP1 inhibition therapy protects against SARS-CoV-2-induced lethal inflammation.

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Article: Topoisomerase 1 inhibition therapy protects against SARS-CoV-2-induced inflammation and death in animal models.

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Article ; Online: Lineage-Specific Genome Architecture Links Enhancers and Non-coding Disease Variants to Target Gene Promoters.

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Article ; Online: Topoisomerase 1 inhibition therapy protects against SARS-CoV-2-induced inflammation and death in animal models.

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Article: Lineage-Specific Genome Architecture Links Enhancers and Non-coding Disease Variants to Target Gene Promoters

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