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Article ; Online: The multicellular interplay of microglia in health and disease: lessons from leukodystrophy.

Berdowski, Woutje M / Sanderson, Leslie E / van Ham, Tjakko J

2021 Volume 14, Issue 8

Abstract: Microglia are highly dynamic cells crucial for developing and maintaining lifelong brain function and health through their many interactions with essentially all cellular components of the central nervous system. The frequent connection of microglia to ... ...

Abstract	Microglia are highly dynamic cells crucial for developing and maintaining lifelong brain function and health through their many interactions with essentially all cellular components of the central nervous system. The frequent connection of microglia to leukodystrophies, genetic disorders of the white matter, has highlighted their involvement in the maintenance of white matter integrity. However, the mechanisms that underlie their putative roles in these processes remain largely uncharacterized. Microglia have also been gaining attention as possible therapeutic targets for many neurological conditions, increasing the demand to understand their broad spectrum of functions and the impact of their dysregulation. In this Review, we compare the pathological features of two groups of genetic leukodystrophies: those in which microglial dysfunction holds a central role, termed 'microgliopathies', and those in which lysosomal or peroxisomal defects are considered to be the primary driver. The latter are suspected to have notable microglia involvement, as some affected individuals benefit from microglia-replenishing therapy. Based on overlapping pathology, we discuss multiple ways through which aberrant microglia could lead to white matter defects and brain dysfunction. We propose that the study of leukodystrophies, and their extensively multicellular pathology, will benefit from complementing analyses of human patient material with the examination of cellular dynamics in vivo using animal models, such as zebrafish. Together, this will yield important insight into the cell biological mechanisms of microglial impact in the central nervous system, particularly in the development and maintenance of myelin, that will facilitate the development of new, and refinement of existing, therapeutic options for a range of brain diseases.
MeSH term(s)	Animals ; Humans ; Microglia/pathology ; Myelin Sheath/pathology ; Neurodegenerative Diseases/pathology ; White Matter/pathology ; Zebrafish
Language	English
Publishing date	2021-07-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.048925
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Article ; Online: CLEC16A interacts with retromer and TRIM27, and its loss impairs endosomal trafficking and neurodevelopment

Smits, Daphne J. / Dekker, Jordy / Schot, Rachel / Tabarki, Brahim / Alhashem, Amal / Demmers, Jeroen A. A. / Dekkers, Dick H. W. / Romito, Antonio / van der Spek, Peter J. / van Ham, Tjakko J. / Bertoli-Avella, Aida M. / Mancini, Grazia M. S.

Hum Genet 2023, v. 142, no. 3, p. 379-397

2023 , Page(s) 379–397

Abstract: CLEC16A is a membrane-associated C-type lectin protein that functions as a E3-ubiquitin ligase. CLEC16A regulates autophagy and mitophagy, and reportedly localizes to late endosomes. GWAS studies have associated CLEC16A SNPs to various auto-immune and ... ...

Abstract	CLEC16A is a membrane-associated C-type lectin protein that functions as a E3-ubiquitin ligase. CLEC16A regulates autophagy and mitophagy, and reportedly localizes to late endosomes. GWAS studies have associated CLEC16A SNPs to various auto-immune and neurological disorders, including multiple sclerosis and Parkinson disease. Studies in mouse models imply a role for CLEC16A in neurodegeneration. We identified bi-allelic CLEC16A truncating variants in siblings from unrelated families presenting with a severe neurodevelopmental disorder including microcephaly, brain atrophy, corpus callosum dysgenesis, and growth retardation. To understand the function of CLEC16A in neurodevelopment we used in vitro models and zebrafish embryos. We observed CLEC16A localization to early endosomes in HEK293T cells. Mass spectrometry of human CLEC16A showed interaction with endosomal retromer complex subunits and the endosomal ubiquitin ligase TRIM27. Expression of the human variant leading to C-terminal truncated CLEC16A, abolishes both its endosomal localization and interaction with TRIM27, suggesting a loss-of-function effect. CLEC16A knockdown increased TRIM27 adhesion to early endosomes and abnormal accumulation of endosomal F-actin, a sign of disrupted vesicle sorting. Mutagenesis of clec16a by CRISPR–Cas9 in zebrafish embryos resulted in accumulated acidic/phagolysosome compartments, in neurons and microglia, and dysregulated mitophagy. The autophagocytic phenotype was rescued by wild-type human CLEC16A but not the C-terminal truncated CLEC16A. Our results demonstrate that CLEC16A closely interacts with retromer components and regulates endosomal fate by fine-tuning levels of TRIM27 and polymerized F-actin on the endosome surface. Dysregulation of CLEC16A-mediated endosomal sorting is associated with neurodegeneration, but it also causes accumulation of autophagosomes and unhealthy mitochondria during brain development.
Keywords	CRISPR-Cas systems ; Danio rerio ; Parkinson disease ; actin ; adhesion ; atrophy ; autophagosomes ; brain ; endosomes ; growth retardation ; humans ; lectins ; loss-of-function mutation ; mass spectrometry ; mice ; mitochondria ; mitophagy ; mutagenesis ; neurodevelopment ; neuroglia ; phenotype ; polymerization ; sclerosis ; ubiquitin-protein ligase
Language	English
Dates of publication	2023-03
Size	p. 379-397
Publishing place	Springer Berlin Heidelberg
Document type	Article ; Online
ZDB-ID	223009-4
ISSN	1432-1203 ; 0340-6717
ISSN (online)	1432-1203
ISSN	0340-6717
DOI	10.1007/s00439-022-02511-3
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Article ; Online: Microglial Activation by Genetically Targeted Conditional Neuronal Ablation in the Zebrafish.

Oosterhof, Nynke / Kuil, Laura E / van Ham, Tjakko J

Methods in molecular biology (Clifton, N.J.)

2016 Volume 1559, Page(s) 377–390

Abstract: In neurodegenerative diseases activation of immune cells is thought to play a major role. Microglia are the main immune cells of the central nervous system. When encountering disease related stimuli microglia adopt an activated phenotype that typically ... ...

Abstract	In neurodegenerative diseases activation of immune cells is thought to play a major role. Microglia are the main immune cells of the central nervous system. When encountering disease related stimuli microglia adopt an activated phenotype that typically includes a rounded morphology. The exact role of microglia or other potentially infiltrating myeloid cells in different brain diseases is not fully understood. In this chapter we present techniques in zebrafish to induce degeneration of neurons, to activate the microglia, and to study activation phenotypes by immunohistochemistry and in vivo by fluorescence microscopic imaging.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Apoptosis/genetics ; Brain/metabolism ; Brain/ultrastructure ; Disease Models, Animal ; Gene Expression ; Genes, Reporter ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Humans ; Immunohistochemistry/methods ; Larva/genetics ; Larva/metabolism ; Larva/ultrastructure ; Luminescent Proteins/genetics ; Luminescent Proteins/metabolism ; Microglia/metabolism ; Microglia/ultrastructure ; Microscopy, Fluorescence/methods ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Neurons/metabolism ; Neurons/ultrastructure ; Phagocytosis ; Phase Transition ; Sepharose/chemistry ; Zebrafish/genetics ; Zebrafish/metabolism ; Red Fluorescent Protein
Chemical Substances	Luminescent Proteins ; Green Fluorescent Proteins (147336-22-9) ; Sepharose (9012-36-6)
Language	English
Publishing date	2016-12-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-6786-5_26
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Article ; Online: Macrophages Do Not Express the Phagocytic Receptor BAI1/

Hsiao, Cheng-Chih / van der Poel, Marlijn / van Ham, Tjakko J / Hamann, Jörg

Frontiers in immunology

2019 Volume 10, Page(s) 962

MeSH term(s)	Angiogenic Proteins/immunology ; Animals ; Humans ; Macrophages/immunology ; Receptors, G-Protein-Coupled/immunology
Chemical Substances	ADGRB1 protein, human ; Angiogenic Proteins ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2019-05-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.00962
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Article ; Online: Unexplained mismatch repair deficiency: Case closed.

Eikenboom, Ellis L / Moen, Sarah / van Leeuwen, Lotte / Geurts-Giele, Willemina R R / Tops, Carli M J / van Ham, Tjakko J / Dinjens, Winand N M / Dubbink, Hendrikus J / Spaander, Manon C W / Wagner, Anja

HGG advances

2022 Volume 4, Issue 1, Page(s) 100167

Abstract: To identify Lynch syndrome (LS) carriers, DNA mismatch repair (MMR) immunohistochemistry (IHC) is performed on colorectal cancers (CRCs). Upon subsequent LS diagnostics, MMR deficiency (MMRd) sometimes remains unexplained (UMMRd). Recently, the ... ...

Abstract	To identify Lynch syndrome (LS) carriers, DNA mismatch repair (MMR) immunohistochemistry (IHC) is performed on colorectal cancers (CRCs). Upon subsequent LS diagnostics, MMR deficiency (MMRd) sometimes remains unexplained (UMMRd). Recently, the importance of complete LS diagnostics to explain UMMRd, involving MMR methylation, germline, and somatic analyses, was stressed. To explore why some MMRd CRCs remain unsolved, we performed a systematic review of the literature and mapped patients with UMMRd diagnosed in our center. A systematic literature search was performed in Ovid Medline, Embase, Web of Science, Cochrane CENTRAL, and Google Scholar for articles on UMMRd CRCs after complete LS diagnostics published until December 15, 2021. Additionally, UMMRd CRCs diagnosed in our center since 1993 were mapped. Of 754 identified articles, 17 were included, covering 74 patients with UMMRd. Five CRCs were microsatellite stable. Upon complete diagnostics, 39 patients had single somatic MMR hits, and six an MMR germline variant of unknown significance (VUS). Ten had somatic pathogenic variants (PVs) in
MeSH term(s)	Humans ; Colorectal Neoplasms/diagnosis ; Neoplastic Syndromes, Hereditary/diagnosis ; Colorectal Neoplasms, Hereditary Nonpolyposis/diagnosis ; Brain Neoplasms
Language	English
Publishing date	2022-12-14
Publishing country	United States
Document type	Systematic Review ; Journal Article
ISSN	2666-2477
ISSN (online)	2666-2477
DOI	10.1016/j.xhgg.2022.100167
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Article ; Online: Immune cell dynamics in the CNS: Learning from the zebrafish.

Oosterhof, Nynke / Boddeke, Erik / van Ham, Tjakko J

Glia

2015 Volume 63, Issue 5, Page(s) 719–735

Abstract: A major question in research on immune responses in the brain is how the timing and nature of these responses influence physiology, pathogenesis or recovery from pathogenic processes. Proper understanding of the immune regulation of the human brain ... ...

Abstract	A major question in research on immune responses in the brain is how the timing and nature of these responses influence physiology, pathogenesis or recovery from pathogenic processes. Proper understanding of the immune regulation of the human brain requires a detailed description of the function and activities of the immune cells in the brain. Zebrafish larvae allow long-term, noninvasive imaging inside the brain at high-spatiotemporal resolution using fluorescent transgenic reporters labeling specific cell populations. Together with recent additional technical advances this allows an unprecedented versatility and scope of future studies. Modeling of human physiology and pathology in zebrafish has already yielded relevant insights into cellular dynamics and function that can be translated to the human clinical situation. For instance, in vivo studies in the zebrafish have provided new insight into immune cell dynamics in granuloma formation in tuberculosis and the mechanisms involving treatment resistance. In this review, we highlight recent findings and novel tools paving the way for basic neuroimmunology research in the zebrafish. GLIA 2015;63:719-735.
MeSH term(s)	Animals ; Central Nervous System/anatomy & histology ; Central Nervous System/immunology ; Humans ; Immune System/cytology ; Immune System/immunology ; Models, Animal ; Neuroglia/physiology ; Nonlinear Dynamics ; Zebrafish/immunology
Language	English
Publishing date	2015-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.22780
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Article ; Online: Biallelic variants in FLII cause pediatric cardiomyopathy by disrupting cardiomyocyte cell adhesion and myofibril organization.

JCI insight

2023 Volume 8, Issue 17

Abstract: Pediatric cardiomyopathy (CM) represents a group of rare, severe disorders that affect the myocardium. To date, the etiology and mechanisms underlying pediatric CM are incompletely understood, hampering accurate diagnosis and individualized therapy ... ...

Abstract	Pediatric cardiomyopathy (CM) represents a group of rare, severe disorders that affect the myocardium. To date, the etiology and mechanisms underlying pediatric CM are incompletely understood, hampering accurate diagnosis and individualized therapy development. Here, we identified biallelic variants in the highly conserved flightless-I (FLII) gene in 3 families with idiopathic, early-onset dilated CM. We demonstrated that patient-specific FLII variants, when brought into the zebrafish genome using CRISPR/Cas9 genome editing, resulted in the manifestation of key aspects of morphological and functional abnormalities of the heart, as observed in our patients. Importantly, using these genetic animal models, complemented with in-depth loss-of-function studies, we provided insights into the function of Flii during ventricular chamber morphogenesis in vivo, including myofibril organization and cardiomyocyte cell adhesion, as well as trabeculation. In addition, we identified Flii function to be important for the regulation of Notch and Hippo signaling, crucial pathways associated with cardiac morphogenesis and function. Taken together, our data provide experimental evidence for a role for FLII in the pathogenesis of pediatric CM and report biallelic variants as a genetic cause of pediatric CM.
MeSH term(s)	Animals ; Cell Adhesion/genetics ; Microfilament Proteins/genetics ; Myocytes, Cardiac/metabolism ; Myofibrils/metabolism ; Zebrafish/genetics ; Trans-Activators ; Cardiomyopathies/genetics
Chemical Substances	Microfilament Proteins ; Trans-Activators
Language	English
Publishing date	2023-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.168247
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Article ; Online: SMPD4 regulates mitotic nuclear envelope dynamics and its loss causes microcephaly and diabetes.

Smits, Daphne J / Schot, Rachel / Krusy, Nathalie / Wiegmann, Katja / Utermöhlen, Olaf / Mulder, Monique T / den Hoedt, Sandra / Yoon, Grace / Deshwar, Ashish R / Kresge, Christina / Pletcher, Beth / van Mook, Maura / Ferreira, Marta Serio / Poot, Raymond A / Slotman, Johan A / Kremers, Gert-Jan / Ahmad, Abeer / Albash, Buthaina / Bastaki, Laila /

Marafi, Dana / Dekker, Jordy / van Ham, Tjakko J / Nguyen, Laurent / Mancini, Grazia M S

Brain : a journal of neurology

2023 Volume 146, Issue 8, Page(s) 3528–3541

Abstract: Biallelic loss-of-function variants in SMPD4 cause a rare and severe neurodevelopmental disorder with progressive congenital microcephaly and early death. SMPD4 encodes a sphingomyelinase that hydrolyses sphingomyelin into ceramide at neutral pH and can ... ...

Abstract	Biallelic loss-of-function variants in SMPD4 cause a rare and severe neurodevelopmental disorder with progressive congenital microcephaly and early death. SMPD4 encodes a sphingomyelinase that hydrolyses sphingomyelin into ceramide at neutral pH and can thereby affect membrane lipid homeostasis. SMPD4 localizes to the membranes of the endoplasmic reticulum and nuclear envelope and interacts with nuclear pore complexes (NPC). We refine the clinical phenotype of loss-of-function SMPD4 variants by describing five individuals from three unrelated families with longitudinal data due to prolonged survival. All individuals surviving beyond infancy developed insulin-dependent diabetes, besides presenting with a severe neurodevelopmental disorder and microcephaly, making diabetes one of the most frequent age-dependent non-cerebral abnormalities. We studied the function of SMPD4 at the cellular and organ levels. Knock-down of SMPD4 in human neural stem cells causes reduced proliferation rates and prolonged mitosis. Moreover, SMPD4 depletion results in abnormal nuclear envelope breakdown and reassembly during mitosis and decreased post-mitotic NPC insertion. Fibroblasts from affected individuals show deficient SMPD4-specific neutral sphingomyelinase activity, without changing (sub)cellular lipidome fractions, which suggests a local function of SMPD4 on the nuclear envelope. In embryonic mouse brain, knockdown of Smpd4 impairs cortical progenitor proliferation and induces premature differentiation by altering the balance between neurogenic and proliferative progenitor cell divisions. We hypothesize that, in individuals with SMPD4-related disease, nuclear envelope bending, which is needed to insert NPCs in the nuclear envelope, is impaired in the absence of SMPD4 and interferes with cerebral corticogenesis and survival of pancreatic beta cells.
MeSH term(s)	Humans ; Animals ; Mice ; Nuclear Envelope/chemistry ; Nuclear Envelope/metabolism ; Microcephaly/genetics ; Microcephaly/metabolism ; Sphingomyelin Phosphodiesterase/analysis ; Sphingomyelin Phosphodiesterase/genetics ; Sphingomyelin Phosphodiesterase/metabolism ; Nuclear Pore/metabolism ; Mitosis ; Diabetes Mellitus/metabolism
Chemical Substances	Sphingomyelin Phosphodiesterase (EC 3.1.4.12)
Language	English
Publishing date	2023-02-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awad033
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Article ; Online: Three patients with defects in interferon gamma receptor signaling: A challenging diagnosis.

Zhou, Zijun / Hollink, Iris H I M / Bouman, Arjan / Lourens, Mirthe S / Brooimans, Rik A / van Ham, Tjakko J / Fraaij, Pieter L A / van Rossum, Annemarie M C / Zijtregtop, Eline A M / Dik, Willem A / Dalm, Virgil A S H / van Hagen, P Martin / Ijspeert, Hanna / Vermont, Clementien L

Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology

2022 Volume 33, Issue 4, Page(s) e13768

MeSH term(s)	Humans ; Receptors, Interferon/genetics ; STAT1 Transcription Factor/metabolism ; Signal Transduction ; Interferon gamma Receptor
Chemical Substances	Receptors, Interferon ; STAT1 Transcription Factor
Language	English
Publishing date	2022-04-01
Publishing country	England
Document type	Letter
ZDB-ID	1057059-7
ISSN	1399-3038 ; 0905-6157 ; 0906-5784
ISSN (online)	1399-3038
ISSN	0905-6157 ; 0906-5784
DOI	10.1111/pai.13768
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Article ; Online: Reduction of oxidative stress suppresses poly-GR-mediated toxicity in zebrafish embryos.

Riemslagh, Fréderike W / Verhagen, Rob F M / van der Toorn, Esmay C / Smits, Daphne J / Quint, Wim H / van der Linde, Herma C / van Ham, Tjakko J / Willemsen, Rob

Disease models & mechanisms

2021 Volume 14, Issue 11

Abstract: The hexanucleotide (G4C2)-repeat expansion in the C9ORF72 gene is the most common pathogenic cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). This repeat expansion can be translated into dipeptide repeat proteins (DPRs), ... ...

Abstract	The hexanucleotide (G4C2)-repeat expansion in the C9ORF72 gene is the most common pathogenic cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). This repeat expansion can be translated into dipeptide repeat proteins (DPRs), and distribution of the poly-GR DPR correlates with neurodegeneration in postmortem C9FTD/ALS brains. Here, we assessed poly-GR toxicity in zebrafish embryos, using an annexin A5-based fluorescent transgenic line (secA5) that allows for detection and quantification of apoptosis in vivo. Microinjection of RNA encoding poly-GR into fertilized oocytes evoked apoptosis in the brain and abnormal motor neuron morphology in the trunk of 1-4-days postfertilization embryos. Poly-GR can be specifically detected in protein homogenates from injected zebrafish and in the frontal cortexes of C9FTD/ALS cases. Poly-GR expression further elevated MitoSOX levels in zebrafish embryos, indicating oxidative stress. Inhibition of reactive oxygen species using Trolox showed full suppression of poly-GR toxicity. Our study indicates that poly-GR can exert its toxicity via oxidative stress. This zebrafish model can be used to find suppressors of poly-GR toxicity and identify its molecular targets underlying neurodegeneration observed in C9FTD/ALS.
MeSH term(s)	Amyotrophic Lateral Sclerosis/pathology ; Animals ; C9orf72 Protein/genetics ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Oxidative Stress ; Zebrafish/metabolism
Chemical Substances	C9orf72 Protein
Language	English
Publishing date	2021-12-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.049092
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