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Article ; Online: Heterochromatin and Polycomb as regulators of haematopoiesis.

Keenan, Christine R

2021 Volume 49, Issue 2, Page(s) 805–814

Abstract: Haematopoiesis is the process by which multipotent haematopoietic stem cells are transformed into each and every type of terminally differentiated blood cell. Epigenetic silencing is critical for this process by regulating the transcription of cell-cycle ...

Abstract	Haematopoiesis is the process by which multipotent haematopoietic stem cells are transformed into each and every type of terminally differentiated blood cell. Epigenetic silencing is critical for this process by regulating the transcription of cell-cycle genes critical for self-renewal and differentiation, as well as restricting alternative fate genes to allow lineage commitment and appropriate differentiation. There are two distinct forms of transcriptionally repressed chromatin: H3K9me3-marked heterochromatin and H3K27me3/H2AK119ub1-marked Polycomb (often referred to as facultative heterochromatin). This review will discuss the role of these distinct epigenetic silencing mechanisms in regulating normal haematopoiesis, how these contribute to age-related haematopoietic dysfunction, and the rationale for therapeutic targeting of these pathways in the treatment of haematological malignancies.
MeSH term(s)	Animals ; Cell Cycle/genetics ; Cell Differentiation/genetics ; Cell Self Renewal ; Chromatin/genetics ; Chromatin/metabolism ; Epigenesis, Genetic ; Hematopoiesis/genetics ; Heterochromatin/genetics ; Heterochromatin/metabolism ; Histones/metabolism ; Humans ; Methylation ; Polycomb-Group Proteins/genetics ; Polycomb-Group Proteins/metabolism
Chemical Substances	Chromatin ; Heterochromatin ; Histones ; Polycomb-Group Proteins
Language	English
Publishing date	2021-05-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20200737
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Article ; Online: Shedding Structured Light on Molecular Immunity: The Past, Present and Future of Immune Cell Super Resolution Microscopy.

Johanson, Timothy M / Keenan, Christine R / Allan, Rhys S

Frontiers in immunology

2021 Volume 12, Page(s) 754200

Abstract: In the two decades since the invention of laser-based super resolution microscopy this family of technologies has revolutionised the way life is viewed and understood. Its unparalleled resolution, speed, and accessibility makes super resolution imaging ... ...

Abstract	In the two decades since the invention of laser-based super resolution microscopy this family of technologies has revolutionised the way life is viewed and understood. Its unparalleled resolution, speed, and accessibility makes super resolution imaging particularly useful in examining the highly complex and dynamic immune system. Here we introduce the super resolution technologies and studies that have already fundamentally changed our understanding of a number of central immunological processes and highlight other immunological puzzles only addressable in super resolution.
MeSH term(s)	Animals ; Cell Lineage ; Equipment Design ; Fluorescence Recovery After Photobleaching ; Humans ; Immune System/cytology ; Immunologic Techniques/instrumentation ; Microscopy, Confocal/instrumentation ; Microscopy, Confocal/methods ; Microscopy, Fluorescence/instrumentation ; Microscopy, Fluorescence/methods ; Receptors, Antigen/ultrastructure ; Receptors, Immunologic/ultrastructure ; Single Molecule Imaging/instrumentation ; Single Molecule Imaging/methods
Chemical Substances	Receptors, Antigen ; Receptors, Immunologic
Language	English
Publishing date	2021-12-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.754200
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Article ; Online: Epigenomic drivers of immune dysfunction in aging.

Keenan, Christine R / Allan, Rhys S

Aging cell

2018 Volume 18, Issue 1, Page(s) e12878

Abstract: Aging inevitably leads to reduced immune function, leaving the elderly more susceptible to infections, less able to respond to pathogen challenges, and less responsive to preventative vaccinations. No cell type is exempt from the ravages of age, and ... ...

Abstract	Aging inevitably leads to reduced immune function, leaving the elderly more susceptible to infections, less able to respond to pathogen challenges, and less responsive to preventative vaccinations. No cell type is exempt from the ravages of age, and extensive studies have found age-related alterations in the frequencies and functions of both stem and progenitor cells, as well as effector cells of both the innate and adaptive immune systems. The intrinsic functional reduction in immune competence is also associated with low-grade chronic inflammation, termed "inflamm-aging," which further perpetuates immune dysfunction. While many of these age-related cellular changes are well characterized, understanding the molecular changes that underpin the functional decline has proven more difficult. Changes in chromatin are increasingly appreciated as a causative mechanism of cellular and organismal aging across species. These changes include increased genomic instability through loss of heterochromatin and increased DNA damage, telomere attrition, and epigenetic alterations. In this review, we discuss the connections between chromatin, immunocompetence, and the loss of function associated with mammalian immune aging. Through understanding the molecular events which underpin the phenotypic changes observed in the aged immune system, it is hoped that the aged immune system can be restored to provide youthful immunity once more.
MeSH term(s)	Aging/genetics ; Aging/immunology ; Chromatin/metabolism ; DNA Methylation/genetics ; Epigenomics ; Genomic Instability ; Humans ; Immune System/physiopathology
Chemical Substances	Chromatin
Language	English
Publishing date	2018-11-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.12878
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Zs.A 6581: Show issues

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Article ; Online: Activation of stably silenced genes by recruitment of a synthetic de-methylating module.

Chan, Wing Fuk / Coughlan, Hannah D / Chen, Yunshun / Keenan, Christine R / Smyth, Gordon K / Perkins, Andrew C / Johanson, Timothy M / Allan, Rhys S

Nature communications

2022 Volume 13, Issue 1, Page(s) 5582

Abstract: Stably silenced genes that display a high level of CpG dinucleotide methylation are refractory to the current generation of dCas9-based activation systems. To counter this, we create an improved activation system by coupling the catalytic domain of DNA ... ...

Abstract	Stably silenced genes that display a high level of CpG dinucleotide methylation are refractory to the current generation of dCas9-based activation systems. To counter this, we create an improved activation system by coupling the catalytic domain of DNA demethylating enzyme TET1 with transcriptional activators (TETact). We show that TETact demethylation-coupled activation is able to induce transcription of suppressed genes, both individually and simultaneously in cells, and has utility across a number of cell types. Furthermore, we show that TETact can effectively reactivate embryonic haemoglobin genes in non-erythroid cells. We anticipate that TETact will expand the existing CRISPR toolbox and be valuable for functional studies, genetic screens and potential therapeutics.
MeSH term(s)	CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; DNA Methylation ; Epigenesis, Genetic ; Promoter Regions, Genetic/genetics ; Transcription Factors/metabolism ; Transcriptional Activation
Chemical Substances	Transcription Factors
Language	English
Publishing date	2022-09-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-33181-4
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Article ; Online: Survey of activation-induced genome architecture reveals a novel enhancer of Myc.

Chan, Wing Fuk / Coughlan, Hannah D / Ruhle, Michelle / Iannarella, Nadia / Alvarado, Carolina / Groom, Joanna R / Keenan, Christine R / Kueh, Andrew J / Wheatley, Adam K / Smyth, Gordon K / Allan, Rhys S / Johanson, Timothy M

Immunology and cell biology

2023 Volume 101, Issue 4, Page(s) 345–357

Abstract: The transcription factor Myc is critically important in driving cell proliferation, a function that is frequently dysregulated in cancer. To avoid this dysregulation Myc is tightly controlled by numerous layers of regulation. One such layer is the use of ...

Abstract	The transcription factor Myc is critically important in driving cell proliferation, a function that is frequently dysregulated in cancer. To avoid this dysregulation Myc is tightly controlled by numerous layers of regulation. One such layer is the use of distal regulatory enhancers to drive Myc expression. Here, using chromosome conformation capture to examine B cells of the immune system in the first hours after their activation, we reveal a previously unidentified enhancer of Myc. The interactivity of this enhancer coincides with a dramatic, but discrete, spike in Myc expression 3 h post-activation. However, genetic deletion of this region, has little impact on Myc expression, Myc protein level or in vitro and in vivo cell proliferation. Examination of the enhancer deleted regulatory landscape suggests that enhancer redundancy likely sustains Myc expression. This work highlights not only the importance of temporally examining enhancers, but also the complexity and dynamics of the regulation of critical genes such as Myc.
MeSH term(s)	Genes, myc ; Enhancer Elements, Genetic/genetics ; Transcription Factors/metabolism ; Gene Expression Regulation ; Promoter Regions, Genetic
Chemical Substances	Transcription Factors
Language	English
Publishing date	2023-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1111/imcb.12626
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Article ; Online: Genome organization in immune cells: unique challenges.

Johanson, Timothy M / Chan, Wing Fuk / Keenan, Christine R / Allan, Rhys S

Nature reviews. Immunology

2019 Volume 19, Issue 7, Page(s) 448–456

Abstract: Each type of cell in the immune system performs critical functions to protect the body and maintain health. In order to fulfil these roles some immune cells rely on unique processes, including antigen receptor loci recombination, clonal expansion or the ... ...

Abstract	Each type of cell in the immune system performs critical functions to protect the body and maintain health. In order to fulfil these roles some immune cells rely on unique processes, including antigen receptor loci recombination, clonal expansion or the contortion of their nuclei. In turn, each of these processes relies on, or poses unique challenges to, a genome organized in three dimensions. Here, we explore the current understanding of the importance of 3D genome organization in the function and development of a healthy immune system.
MeSH term(s)	Alleles ; Animals ; Genome ; Humans ; Immune System/physiology ; Receptors, Antigen, T-Cell/genetics ; Recombination, Genetic
Chemical Substances	Receptors, Antigen, T-Cell
Language	English
Publishing date	2019-03-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2062776-2
ISSN	1474-1741 ; 1474-1733
ISSN (online)	1474-1741
ISSN	1474-1733
DOI	10.1038/s41577-019-0155-2
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Zs.A 5565: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 34: Show issues

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Article ; Online: Biased signalling from the glucocorticoid receptor: Renewed opportunity for tailoring glucocorticoid activity.

Keenan, Christine R / Lew, Michael J / Stewart, Alastair G

Biochemical pharmacology

2016 Volume 112, Page(s) 6–12

Abstract: Recent landmark studies applying analytical pharmacology approaches to the glucocorticoid receptor (GR) have demonstrated that different ligands can cause differential activation of distinct GR-regulated genes. Drawing on concepts of signalling bias from ...

Abstract	Recent landmark studies applying analytical pharmacology approaches to the glucocorticoid receptor (GR) have demonstrated that different ligands can cause differential activation of distinct GR-regulated genes. Drawing on concepts of signalling bias from the field of G protein-coupled receptor (GPCR) biology, we speculate that ligand-dependent differences in GR signalling can be considered analogous to GPCR biased signalling, and thus can be quantitatively analysed in a similar way. This type of approach opens up the possibility of using rational structure-based drug optimisation strategies to improve the therapeutic selectivity of glucocorticoid drugs to maximise their efficacy and minimise adverse effects.
MeSH term(s)	Animals ; Glucocorticoids/adverse effects ; Glucocorticoids/chemistry ; Glucocorticoids/pharmacology ; Humans ; Ligands ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Glucocorticoid/genetics ; Receptors, Glucocorticoid/metabolism ; Signal Transduction/drug effects ; Structure-Activity Relationship
Chemical Substances	Glucocorticoids ; Ligands ; Receptors, G-Protein-Coupled ; Receptors, Glucocorticoid
Language	English
Publishing date	2016-07-15
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2016.02.008
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Zs.A 19: Show issues

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Article ; Online: Identification and characterization of the long noncoding RNA Dreg1 as a novel regulator of Gata3.

Chan, Wing Fuk / Coughlan, Hannah D / Iannarella, Nadia / Smyth, Gordon K / Johanson, Timothy M / Keenan, Christine R / Allan, Rhys S

Immunology and cell biology

2020 Volume 99, Issue 3, Page(s) 323–332

Abstract: The eukaryotic genome is three-dimensionally segregated into discrete globules of topologically associating domains (TADs), within which numerous cis-regulatory elements such as enhancers and promoters interact to regulate gene expression. In this study, ...

Abstract	The eukaryotic genome is three-dimensionally segregated into discrete globules of topologically associating domains (TADs), within which numerous cis-regulatory elements such as enhancers and promoters interact to regulate gene expression. In this study, we identify a T-cell-specific sub-TAD containing the Gata3 locus, and reveal a previously uncharacterized long noncoding RNA (Dreg1) within a distant enhancer lying approximately 280 kb downstream of Gata3. Dreg1 expression is highly correlated with that of Gata3 during early immune system development and T helper type 2 cell differentiation. Inhibition and overexpression of Dreg1 suggest that it may be involved in the establishment, but not in the maintenance of Gata3 expression. Overall, we propose that Dreg1 is a novel regulator of Gata3 and may inform therapeutic strategies in diseases such allergy and lymphoma, where Gata3 has a pathological role.
MeSH term(s)	Chromatin ; Enhancer Elements, Genetic/genetics ; GATA3 Transcription Factor/genetics ; GATA3 Transcription Factor/metabolism ; Promoter Regions, Genetic ; RNA, Long Noncoding/genetics
Chemical Substances	Chromatin ; GATA3 Transcription Factor ; RNA, Long Noncoding
Language	English
Publishing date	2020-10-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1111/imcb.12408
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Article ; Online: Pro-inflammatory mediators increase levels of the noncoding RNA GAS5 in airway smooth muscle and epithelial cells.

Keenan, Christine R / Schuliga, Michael J / Stewart, Alastair G

Canadian journal of physiology and pharmacology

2015 Volume 93, Issue 3, Page(s) 203–206

Abstract: The long noncoding RNA (lncRNA) GAS5 has been found to act as a decoy for the glucocorticoid receptor (GR), thus implicating GAS5 as a potential regulator of glucocorticoid sensitivity and resistance. Airway smooth muscle (ASM) cells and airway ... ...

Abstract	The long noncoding RNA (lncRNA) GAS5 has been found to act as a decoy for the glucocorticoid receptor (GR), thus implicating GAS5 as a potential regulator of glucocorticoid sensitivity and resistance. Airway smooth muscle (ASM) cells and airway epithelial cells (AEC) play an important role in the pathogenesis and persistence of asthma and other chronic airways diseases. These airway structural cell types are also important cellular targets of the anti-inflammatory actions of glucocorticoids. In this study, we sought to examine the relevance of GAS5 to glucocorticoid sensitivity and resistance in ASM and AEC. We provide the first evidence that pro-inflammatory mediators up-regulate GAS5 levels in both airway epithelial and smooth muscle cells, and that decreasing GAS5 levels can enhance glucocorticoid action in AEC.
MeSH term(s)	Anti-Inflammatory Agents/pharmacology ; Cell Line ; Cytokines/metabolism ; Dexamethasone/pharmacology ; Epithelial Cells/metabolism ; Humans ; Inflammation/metabolism ; Lung/metabolism ; Mifepristone/pharmacology ; Muscle, Smooth/metabolism ; RNA, Long Noncoding/metabolism ; Up-Regulation/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Cytokines ; GAS5 long non-coding RNA, human ; RNA, Long Noncoding ; Mifepristone (320T6RNW1F) ; Dexamethasone (7S5I7G3JQL)
Language	English
Publishing date	2015-03
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	127527-6
ISSN	1205-7541 ; 0008-4212
ISSN (online)	1205-7541
ISSN	0008-4212
DOI	10.1139/cjpp-2014-0391
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Zs.A 589: Show issues

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Article ; Online: Extreme disruption of heterochromatin is required for accelerated hematopoietic aging.

Keenan, Christine R / Iannarella, Nadia / Naselli, Gaetano / Bediaga, Naiara G / Johanson, Timothy M / Harrison, Leonard C / Allan, Rhys S

Blood

2020 Volume 135, Issue 23, Page(s) 2049–2058

Abstract: Loss of heterochromatin has been proposed as a universal mechanism of aging across different species and cell types. However, a comprehensive analysis of hematopoietic changes caused by heterochromatin loss is lacking. Moreover, there is conflict in the ... ...

Abstract	Loss of heterochromatin has been proposed as a universal mechanism of aging across different species and cell types. However, a comprehensive analysis of hematopoietic changes caused by heterochromatin loss is lacking. Moreover, there is conflict in the literature around the role of the major heterochromatic histone methyltransferase Suv39h1 in the aging process. Here, we use individual and dual deletion of Suv39h1 and Suv39h2 enzymes to examine the causal role of heterochromatin loss in hematopoietic cell development. Loss of neither Suv39h1 nor Suv39h2 individually had any effect on hematopoietic stem cell function or the development of mature lymphoid or myeloid lineages. However, deletion of both enzymes resulted in characteristic changes associated with aging such as reduced hematopoietic stem cell function, thymic involution and decreased lymphoid output with a skewing toward myeloid development, and increased memory T cells at the expense of naive T cells. These cellular changes were accompanied by molecular changes consistent with aging, including alterations in nuclear shape and increased nucleolar size. Together, our results indicate that the hematopoietic system has a remarkable tolerance for major disruptions in chromatin structure and reveal a role for Suv39h2 in depositing sufficient H3K9me3 to protect the entire hematopoietic system from changes associated with premature aging.
MeSH term(s)	Aged ; Aging, Premature/metabolism ; Aging, Premature/pathology ; Animals ; Cell Differentiation ; Cell Nucleus/genetics ; Female ; Hematopoiesis ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; Heterochromatin/genetics ; Heterochromatin/metabolism ; Histone-Lysine N-Methyltransferase/physiology ; Humans ; Male ; Methyltransferases/physiology ; Mice ; Mice, Knockout ; Repressor Proteins/physiology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology
Chemical Substances	Heterochromatin ; Repressor Proteins ; Suv39h1 protein, mouse (EC 2.1.1.) ; Methyltransferases (EC 2.1.1.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Suv39h2 protein, mouse (EC 2.1.1.43)
Language	English
Publishing date	2020-04-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2019002990
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Uh III Zs.140: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 364: Show issues

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