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Article ; Online: CCAAT enhancer binding protein alpha (CEBPA) biallelic acute myeloid leukaemia: cooperating lesions, molecular mechanisms and clinical relevance.

Wilhelmson, Anna S / Porse, Bo T

2020 Volume 190, Issue 4, Page(s) 495–507

Abstract: Recent advances in sequencing technologies have allowed for the identification of recurrent mutations in acute myeloid leukaemia (AML). The transcription factor CCAAT enhancer binding protein alpha (CEBPA) is frequently mutated in AML, and biallelic ... ...

Abstract	Recent advances in sequencing technologies have allowed for the identification of recurrent mutations in acute myeloid leukaemia (AML). The transcription factor CCAAT enhancer binding protein alpha (CEBPA) is frequently mutated in AML, and biallelic CEBPA-mutant AML was recognised as a separate disease entity in the recent World Health Organization classification. However, CEBPA mutations are co-occurring with other aberrations in AML, and together these lesions form the clonal hierarchy that comprises the leukaemia in the patient. Here, we aim to review the current understanding of co-occurring mutations in CEBPA-mutated AML and their implications for disease biology and clinical outcome. We will put emphasis on patterns of cooperation, how these lesions cooperate with CEBPA mutations and the underlying potential molecular mechanisms. Finally, we will relate this to patient outcome and future options for personalised medicine.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Alleles ; CCAAT-Enhancer-Binding Proteins/genetics ; CCAAT-Enhancer-Binding Proteins/physiology ; Child ; Child, Preschool ; Clonal Evolution ; DNA Methylation ; Female ; Histone Code ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/physiology ; Leukemia, Myeloid, Acute/classification ; Leukemia, Myeloid, Acute/genetics ; Male ; Middle Aged ; Mutation ; Neoplasm Proteins/genetics ; Neoplasm Proteins/physiology ; Precision Medicine ; RNA Splicing Factors/genetics ; RNA Splicing Factors/physiology ; Recurrence ; Transcription Factors/genetics ; Transcription Factors/physiology ; Treatment Outcome ; Young Adult
Chemical Substances	CCAAT-Enhancer-Binding Proteins ; CEBPA protein, human ; Intracellular Signaling Peptides and Proteins ; Neoplasm Proteins ; RNA Splicing Factors ; Transcription Factors
Language	English
Publishing date	2020-02-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/bjh.16534
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Article: Proinflammatory Cytokines Suppress Nonsense-Mediated RNA Decay to Impair Regulated Transcript Isoform Processing in Pancreatic β-Cells.

Ghiasi, Seyed M / Marchetti, Piero / Piemonti, Lorenzo / Nielsen, Jens H / Porse, Bo T / Mandrup-Poulsen, Thomas / Rutter, Guy A

bioRxiv : the preprint server for biology

2024

Abstract: Proinflammatory cytokines are implicated in pancreatic β-cell failure in type 1 and type 2 diabetes and are known to stimulate alternative RNA splicing and the expression of Nonsense-Mediated RNA Decay (NMD) components. Here, we investigate whether ... ...

Abstract	Proinflammatory cytokines are implicated in pancreatic β-cell failure in type 1 and type 2 diabetes and are known to stimulate alternative RNA splicing and the expression of Nonsense-Mediated RNA Decay (NMD) components. Here, we investigate whether cytokines regulate NMD activity and identify transcript isoforms targeted in β-cells. A luciferase-based NMD reporter transiently expressed in rat INS1(832/13), human-derived EndoC-βH3 or dispersed human islet cells is used to examine the effect of proinflammatory cytokines (Cyt) on NMD activity. Gain- or loss-of function of two key NMD components UPF3B and UPF2 is used to reveal the effect of cytokines on cell viability and function. RNA-sequencing and siRNA-mediated silencing are deployed using standard techniques. Cyt attenuate NMD activity in insulin-producing cell lines and primary human β-cells. These effects are found to involve ER stress and are associated with downregulation of UPF3B. Increases or decreases in NMD activity achieved by UPF3B overexpression (OE) or UPF2 silencing, raises or lowers Cyt-induced cell death, respectively, in EndoC-βH3 cells, and are associated with decreased or increased insulin content, respectively. No effects of these manipulations are observed on glucose-stimulated insulin secretion. Transcriptomic analysis reveals that Cyt increase alternative splicing (AS)-induced exon skipping in the transcript isoforms, and this is potentiated by UPF2 silencing. Gene enrichment analysis identifies transcripts regulated by UPF2 silencing whose proteins are localized and/or functional in extracellular matrix (ECM) including the serine protease inhibitor SERPINA1/α-1-antitrypsin, whose silencing sensitises β-cells to Cyt cytotoxicity. Cytokines suppress NMD activity via UPR signalling, potentially serving as a protective response against Cyt-induced NMD component expression. Our findings highlight the central importance of RNA turnover in β-cell responses to inflammatory stress.
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.12.20.572623
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Article: Proinflammatory cytokines suppress nonsense-mediated RNA decay to impair regulated transcript isoform processing in pancreatic β cells.

Ghiasi, Seyed M / Marchetti, Piero / Piemonti, Lorenzo / Nielsen, Jens H / Porse, Bo T / Mandrup-Poulsen, Thomas / Rutter, Guy A

Frontiers in endocrinology

2024 Volume 15, Page(s) 1359147

Abstract: Introduction: Proinflammatory cytokines are implicated in pancreatic ß cell failure in type 1 and type 2 diabetes and are known to stimulate alternative RNA splicing and the expression of nonsense-mediated RNA decay (NMD) components. Here, we ... ...

Abstract	Introduction: Proinflammatory cytokines are implicated in pancreatic ß cell failure in type 1 and type 2 diabetes and are known to stimulate alternative RNA splicing and the expression of nonsense-mediated RNA decay (NMD) components. Here, we investigate whether cytokines regulate NMD activity and identify transcript isoforms targeted in ß cells. Methods: A luciferase-based NMD reporter transiently expressed in rat INS1(832/13), human-derived EndoC-ßH3, or dispersed human islet cells is used to examine the effect of proinflammatory cytokines (Cyt) on NMD activity. The gain- or loss-of-function of two key NMD components, UPF3B and UPF2, is used to reveal the effect of cytokines on cell viability and function. RNA-sequencing and siRNA-mediated silencing are deployed using standard techniques. Results: Cyt attenuate NMD activity in insulin-producing cell lines and primary human ß cells. These effects are found to involve ER stress and are associated with the downregulation of UPF3B. Increases or decreases in NMD activity achieved by UPF3B overexpression (OE) or UPF2 silencing raise or lower Cyt-induced cell death, respectively, in EndoC-ßH3 cells and are associated with decreased or increased insulin content, respectively. No effects of these manipulations are observed on glucose-stimulated insulin secretion. Transcriptomic analysis reveals that Cyt increases alternative splicing (AS)-induced exon skipping in the transcript isoforms, and this is potentiated by UPF2 silencing. Gene enrichment analysis identifies transcripts regulated by UPF2 silencing whose proteins are localized and/or functional in the extracellular matrix (ECM), including the serine protease inhibitor SERPINA1/α-1-antitrypsin, whose silencing sensitizes ß-cells to Cyt cytotoxicity. Cytokines suppress NMD activity via UPR signaling, potentially serving as a protective response against Cyt-induced NMD component expression. Conclusion: Our findings highlight the central importance of RNA turnover in ß cell responses to inflammatory stress.
MeSH term(s)	Humans ; Rats ; Animals ; RNA/metabolism ; Insulin-Secreting Cells/metabolism ; Cytokines/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Nonsense Mediated mRNA Decay ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Insulins/metabolism ; RNA-Binding Proteins/genetics
Chemical Substances	RNA (63231-63-0) ; Cytokines ; Protein Isoforms ; Insulins ; UPF3B protein, human ; RNA-Binding Proteins
Language	English
Publishing date	2024-03-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2024.1359147
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Article ; Online: Myelodysplastic syndrome patient-derived xenografts: from no options to many.

Côme, Christophe / Balhuizen, Alexander / Bonnet, Dominique / Porse, Bo T

Haematologica

2020 Volume 105, Issue 4, Page(s) 864–869

MeSH term(s)	Animals ; Disease Models, Animal ; Heterografts ; Humans ; Myelodysplastic Syndromes/genetics
Language	English
Publishing date	2020-03-19
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2019.233320
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Article ; Online: Real-Time Search-Assisted Acquisition on a Tribrid Mass Spectrometer Improves Coverage in Multiplexed Single-Cell Proteomics.

Furtwängler, Benjamin / Üresin, Nil / Motamedchaboki, Khatereh / Huguet, Romain / Lopez-Ferrer, Daniel / Zabrouskov, Vlad / Porse, Bo T / Schoof, Erwin M

Molecular & cellular proteomics : MCP

2022 Volume 21, Issue 4, Page(s) 100219

Abstract: In the young field of single-cell proteomics (scMS), there is a great need for improved global proteome characterization, both in terms of proteins quantified per cell and quantitative performance thereof. The recently introduced real-time search (RTS) ... ...

Abstract	In the young field of single-cell proteomics (scMS), there is a great need for improved global proteome characterization, both in terms of proteins quantified per cell and quantitative performance thereof. The recently introduced real-time search (RTS) on the Orbitrap Eclipse Tribrid mass spectrometer in combination with SPS-MS3 acquisition has been shown to be beneficial for the measurement of samples that are multiplexed using isobaric tags. Multiplexed scMS requires high ion injection times and high-resolution spectra to quantify the single-cell signal; however, the carrier channel facilitates peptide identification and thus offers the opportunity for fast on-the-fly precursor filtering before committing to the time-intensive quantification scan. Here, we compared classical MS2 acquisition against RTS-SPS-MS3, both using the Orbitrap Eclipse Tribrid MS with the FAIMS Pro ion mobility interface and present a new acquisition strategy termed RETICLE (RTS enhanced quant of single cell spectra) that makes use of fast real-time searched linear ion trap scans to preselect MS1 peptide precursors for quantitative MS2 Orbitrap acquisition. We show that classical MS2 acquisition is outperformed by both RTS-SPS-MS3 through increased quantitative accuracy at similar proteome coverage, and RETICLE through higher proteome coverage, with the latter enabling the quantification of over 1000 proteins per cell at an MS2 injection time of 750 ms using a 2 h gradient.
MeSH term(s)	Mass Spectrometry ; Peptides ; Proteome ; Proteomics
Chemical Substances	Peptides ; Proteome
Language	English
Publishing date	2022-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2075924-1
ISSN	1535-9484 ; 1535-9476
ISSN (online)	1535-9484
ISSN	1535-9476
DOI	10.1016/j.mcpro.2022.100219
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Article ; Online: Heterozygous loss of Srp72 in mice is not associated with major hematological phenotypes.

D'Altri, Teresa / Schuster, Mikkel B / Wenzel, Anne / Porse, Bo T

European journal of haematology

2019 Volume 103, Issue 4, Page(s) 319–328

Abstract: Objectives: Familial cases of hematological malignancies are associated with germline mutations. In particular, heterozygous mutations of SRP72 correlate with the development of myelodysplasia and bone marrow aplasia in two families. The signal ... ...

Abstract	Objectives: Familial cases of hematological malignancies are associated with germline mutations. In particular, heterozygous mutations of SRP72 correlate with the development of myelodysplasia and bone marrow aplasia in two families. The signal recognition particle 72 kDa protein (SRP72) is part of the SRP complex, responsible for targeting of proteins to the endoplasmic reticulum. The main objective of this study is to investigate the role of SRP72 in the hematopoietic system, thus explaining why a reduced dose could increase susceptibility to hematological malignancies. Methods: We developed an Srp72 null mouse model and characterized its hematopoietic system using flow cytometry, bone marrow transplantations, and gene expression analysis. Results: Heterozygous loss of Srp72 in mice is not associated with major changes in hematopoiesis, although causes mild reductions in blood and BM cellularity and minor changes within the stem/progenitor compartment. We did not observe any hematological disorder. Interestingly, gene expression analysis demonstrated that genes encoding secreted factors, including cytokines and receptors, were transcriptionally down-regulated in Srp72 Conclusions: The Srp72
MeSH term(s)	Animals ; Biomarkers ; Blood Cell Count ; Bone Marrow/pathology ; Disease Models, Animal ; Gene Editing ; Gene Expression ; Genes, Lethal ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype ; Hematopoiesis/genetics ; Loss of Heterozygosity ; Mice ; Mice, Knockout ; Mutation ; Phenotype ; Signal Recognition Particle/genetics
Chemical Substances	Biomarkers ; Signal Recognition Particle ; Srp72 protein, mouse
Language	English
Publishing date	2019-07-26
Publishing country	England
Document type	Journal Article
ZDB-ID	392482-8
ISSN	1600-0609 ; 0902-4441
ISSN (online)	1600-0609
ISSN	0902-4441
DOI	10.1111/ejh.13286
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Article ; Online: The functional consequences of intron retention: alternative splicing coupled to NMD as a regulator of gene expression.

Ge, Ying / Porse, Bo T

BioEssays : news and reviews in molecular, cellular and developmental biology

2014 Volume 36, Issue 3, Page(s) 236–243

Abstract: The explosion in sequencing technologies has provided us with an instrument to describe mammalian transcriptomes at unprecedented depths. This has revealed that alternative splicing is used extensively not only to generate protein diversity, but also as ... ...

Abstract	The explosion in sequencing technologies has provided us with an instrument to describe mammalian transcriptomes at unprecedented depths. This has revealed that alternative splicing is used extensively not only to generate protein diversity, but also as a means to regulate gene expression post-transcriptionally. Intron retention (IR) is overwhelmingly perceived as an aberrant splicing event with little or no functional consequence. However, recent work has now shown that IR is used to regulate a specific differentiation event within the haematopoietic system by coupling it to nonsense-mediated mRNA decay (NMD). Here, we highlight how IR and, more broadly, alternative splicing coupled to NMD (AS-NMD) can be used to regulate gene expression and how this is deregulated in disease. We suggest that the importance of AS-NMD is not restricted to the haematopoietic system but that it plays a prominent role in other normal and aberrant biological settings.
MeSH term(s)	Alternative Splicing/genetics ; Animals ; Cell Differentiation/genetics ; Disease/genetics ; Granulocytes/cytology ; Granulocytes/metabolism ; Humans ; Introns/genetics ; Nonsense Mediated mRNA Decay/genetics
Language	English
Publishing date	2014-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.201300156
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Article ; Online: Corrigendum: The Polycomb group proteins bind throughout the

Bracken, Adrian P / Kleine-Kohlbrecher, Daniela / Dietrich, Nikolaj / Pasini, Diego / Gargiulo, Gaetano / Beekman, Chantal / Theilgaard-Mönch, Kim / Minucci, Saverio / Porse, Bo T / Marine, Jean-Christophe / Hansen, Klaus H / Helin, Kristian

Genes & development

2023 Volume 37, Issue 17-18, Page(s) 861

Language	English
Publishing date	2023-10-18
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.351178.123
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Article ; Online: ERG Functionally Overlaps with Other Ets Proteins in Promoting TH9 Cell Expression of Il9 during Allergic Lung Inflammation.

Kharwadkar, Rakshin / Ulrich, Benjamin J / Chu, Michelle / Koh, Byunghee / Hufford, Matthew M / Fu, Yongyao / Birdsey, Graeme M / Porse, Bo T / Randi, Anna M / Kaplan, Mark H

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 210, Issue 5, Page(s) 537–546

Abstract: CD4+ TH cells develop into subsets that are specialized in the secretion of particular cytokines to mediate restricted types of inflammation and immune responses. Among the subsets that promote development of allergic inflammatory responses, IL-9- ... ...

Abstract	CD4+ TH cells develop into subsets that are specialized in the secretion of particular cytokines to mediate restricted types of inflammation and immune responses. Among the subsets that promote development of allergic inflammatory responses, IL-9-producing TH9 cells are regulated by a number of transcription factors. We have previously shown that the E26 transformation-specific (Ets) family members PU.1 and Ets translocation variant 5 (ETV5) function in parallel to regulate IL-9. In this study we identified a third member of the Ets family of transcription factors, Ets-related gene (ERG), that mediates IL-9 production in TH9 cells in the absence of PU.1 and ETV5. Chromatin immunoprecipitation assays revealed that ERG interaction at the Il9 promoter region is restricted to the TH9 lineage and is sustained during murine TH9 polarization. Knockdown or knockout of ERG during murine or human TH9 polarization in vitro led to a decrease in IL-9 production in TH9 cells. Deletion of ERG in vivo had modest effects on IL-9 production in vitro or in vivo. However, in the absence of PU.1 and ETV5, ERG was required for residual IL-9 production in vitro and for IL-9 production by lung-derived CD4 T cells in a mouse model of chronic allergic airway disease. Thus, ERG contributes to IL-9 regulation in TH9 cells.
MeSH term(s)	Animals ; Humans ; Mice ; Alveolitis, Extrinsic Allergic ; Asthma ; CD4-Positive T-Lymphocytes ; Cell Differentiation ; Hypersensitivity ; Interleukin-9 ; Pneumonia/metabolism ; T-Lymphocytes, Helper-Inducer ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcriptional Regulator ERG/metabolism
Chemical Substances	ERG protein, human ; Interleukin-9 ; Transcription Factors ; Transcriptional Regulator ERG ; ERG protein, mouse ; IL9 protein, human
Language	English
Publishing date	2023-01-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2200113
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Article ; Online: The ASXL1-G643W variant accelerates the development of CEBPA mutant acute myeloid leukemia.

D'Altri, Teresa / Wilhelmson, Anna S / Schuster, Mikkel B / Wenzel, Anne / Kalvisa, Adrija / Pundhir, Sachin / Meldgaard Hansen, Anne / Porse, Bo T

Haematologica

2021 Volume 106, Issue 4, Page(s) 1000–1007

Abstract: ASXL1 is one of the most commonly mutated genes in myeloid malignancies, including Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML). In order to further our understanding of the role of ASXL1 lesions in malignant hematopoiesis, we ... ...

Abstract	ASXL1 is one of the most commonly mutated genes in myeloid malignancies, including Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML). In order to further our understanding of the role of ASXL1 lesions in malignant hematopoiesis, we generated a novel knock-in mouse model carrying the most frequent ASXL1 mutation identified in MDS patients, p.G643WfsX12. Mutant mice did not display any major hematopoietic defects nor developed any apparent hematological disease. In AML patients, ASXL1 mutations co-occur with mutations in CEBPA and we therefore generated compound Cebpa and Asxl1 mutated mice. Using a transplantation model, we found that the mutated Asxl1 allele significantly accelerated disease development in a CEBPA mutant context. Importantly, we demonstrated that, similar to the human setting, Asxl1 mutated mice responded poorly to chemotherapy. This model therefore constitutes an excellent experimental system for further studies into the clinically important question of chemotherapy resistance mediated by mutant ASXL1.
MeSH term(s)	Animals ; CCAAT-Enhancer-Binding Proteins ; Hematopoiesis ; Humans ; Leukemia, Myeloid, Acute/genetics ; Mice ; Mutation ; Myelodysplastic Syndromes/genetics ; Myeloproliferative Disorders ; Repressor Proteins/genetics
Chemical Substances	ASXL1 protein, human ; Asxl1 protein, mouse ; CCAAT-Enhancer-Binding Proteins ; CEBPA protein, human ; CEBPA protein, mouse ; Repressor Proteins
Language	English
Publishing date	2021-04-01
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2019.235150
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