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Koopmans, F.

Publications and source records attributed to Koopmans, F..

5 recordsLinked to original sources

The TREM-receptor family interactome in the human brain

The Triggering Receptors Expressed on Myeloid cells (TREMs) are a family of cell-surface receptors instrumental in the activation of different myeloid cells. TREM2, its most studied member, is genetically linked to Alzheimer disease (AD), and its interactions with BAmyloid; and APOE have placed it at the forefront of microglia dysfunction in the brain. However, the ligands and binding partners of the other TREM members (TREM1, TREML1, TREML2 and TREML4) are less well defined. Here, we used human AD and non-AD brain lysate to profile the interactome of the ligand binding domains of the different TREM receptors. Besides identifying known ligands for TREM1 (PGLYRP1), TREM2 (C1QL3, LGALSL) and TREML1 (Fibrinogens), we identified complement components and the apolipoproteins APOA1 and APOA4 as novel interactors of TREML1, and heparan sulfate modified proteins as binding partners for TREML2. Furthermore, similar to TREM2, all the TREMLs interacted with the apolipoproteins APOE and Clusterin. Using in vitro pulldowns with heparin, we confirmed that specifically TREML2 interacted with heparan sulfates, in a manner unaffected by the AD-linked S144G mutation. Together, our proteomics approach identified novel interactors for TREML1 and TREML2, cementing the role of the different TREM-proteins in lipid trafficking and immunity.

neuroscience↗

NREM Oscillations Mediate Synaptic Proteome Remodelling to Support Synapse Stabilisation

Synapses are known to remodel their proteome during sleep. However, the exact mechanisms driving this remodelling and its impact on synaptic function or cognition are not well understood. We combine 24-hour EEG recordings with time-resolved synaptic proteomics in a model of SYNGAP1-Related Disorders to reveal a mechanism by which slow-waves and spindles, two NREM sleep oscillations, mediate the remodelling of the synaptic proteome. Moreover, we uncover that this remodelling promotes synaptic stabilization, which could support sleep-dependent memory consolidation. In contrast, the increase of slow-waves and decrease of spindles found in Syngap1+/- mice would activate molecular pathways involved in synaptic weakening instead of stabilization. This is consistent with the proposed roles of slow-waves and spindles in synaptic downscaling and potentiation, respectively. Here, we provide evidence on how NREM oscillations regulate the synaptic proteome and reveal a pathological mechanism that could be of relevance to all neurodevelopmental disorders coursing with sleep disturbances.

neuroscience↗

One-step induction of human GABAergic neurons promotes presynaptic development & synapse maturation

Human induced pluripotent stem cells (iPSCs) present a powerful approach to study human brain physiology and disease, yet robust, pure GABAergic induction has remained difficult. Here we present improved, single-step, transposon-based GABAergic induction with Ascl1/Dlx2, which yields, unlike lentiviral approaches, exclusively GABAergic neurons and was validated across three independent iPSC lines. Co-seeding with Ngn2-induced excitatory neurons created stable networks of predefined excitation/inhibition ratios, with corresponding synapse ratios. Proteomic and electrophysiological characterization at different developmental time points showed that the single-step induced GABAergic neurons gain a proteomic profile that maps to different cortical interneuron subtypes and display typical GABAergic synaptic properties, producing large, synchronous and picrotoxin-sensitive currents. During early development, synaptic strength increased threefold, which was accompanied by an increase in expression of proteins exclusively enriched for presynaptic SYNGO terms. Synaptic strength continued to increase during late development but with only minor proteomic changes. Taken together, transposon-based GABAergic induction yields exclusively mature GABAergic neurons suitable for studying genes involved in synaptic maturation and to build excitation/inhibition networks for disease modelling.

neuroscience↗

GOAT: efficient and robust identification of geneset enrichment

Geneset enrichment analysis is foundational to the interpretation of high throughput biology. We here present GOAT (https://ftwkoopmans.github.io/goat), a parameter-free permutation-based algorithm for geneset enrichment analysis of preranked genelists. Estimated geneset p-values are well calibrated under the null hypothesis and invariant to geneset size. GOAT consistently identifies more Gene Ontology terms in real-world datasets than current methods and is available as an R package and online tool.

bioinformatics↗

Single-cell isoform RNA sequencing (ScISOr-Seq) across thousands of cells reveals isoforms of cerebellar cell types.

Full-length isoform sequencing has advanced our knowledge of isoform biology1-11. However, apart from applying full-length isoform sequencing to very few single cells12,13, isoform sequencing has been limited to bulk tissue, cell lines, or sorted cells. Single splicing events have been described for <=200 single cells with great statistical success14,15, but these methods do not describe full-length mRNAs. Single cell short-read 3 sequencing has allowed identification of many cell sub-types16-23, but full-length isoforms for these cell types have not been profiled. Using our new method of single-cell-isoform-RNA-sequencing (ScISOr-Seq) we determine isoform-expression in thousands of individual cells from a heterogeneous bulk tissue (cerebellum), without specific antibody-fluorescence activated cell sorting. We elucidate isoform usage in high-level cell types such as neurons, astrocytes and microglia and finer sub-types, such as Purkinje cells and Granule cells, including the combination patterns of distant splice sites6-9,24,25, which for individual molecules requires long reads. We produce an enhanced genome annotation revealing cell-type specific expression of known and 16,872 novel (with respect to mouse Gencode version 10) isoforms (see isoformatlas.com).\n\nScISOr-Seq describes isoforms from >1,000 single cells from bulk tissue without cell sorting by leveraging two technologies in three steps: In step one, we employ microfluidics to produce amplified full-length cDNAs barcoded for their cell of origin. This cDNA is split into two pools: one pool for 3 sequencing to measure gene expression (step 2) and another pool for long-read sequencing and isoform expression (step 3). In step two, short-read 3-sequencing provides molecular counts for each gene and cell, which allows clustering cells and assigning a cell type using cell-type specific markers. In step three, an aliquot of the same cDNAs (each barcoded for the individual cell of origin) is sequenced using Pacific Biosciences (\"PacBio\")1,2,4,5,26 or Oxford Nanopore3. Since these long reads carry the single-cell barcodes identified in step two, one can determine the individual cell from which each long read originates. Since most single cells are assigned to a named cluster, we can also assign the cells cluster name (e.g. \"Purkinje cell\" or \"astrocyte\") to the long read in question (Fig 1A) - without losing the cell of origin of each long read.\n\nO_FIG O_LINKSMALLFIG WIDTH=180 HEIGHT=200 SRC=\"FIGDIR/small/364950_fig1.gif\" ALT=\"Figure 1\">\nView larger version (66K):\norg.highwire.dtl.DTLVardef@4df0cdorg.highwire.dtl.DTLVardef@fc4beborg.highwire.dtl.DTLVardef@1dc485forg.highwire.dtl.DTLVardef@1138a3e_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 1:C_FLOATNO (A) Outline of our ScISOr-Seq approach. (B) TSNE-plot depicting cell clusters, marker genes and names given to clusters, including: Bergman glia (BG), External granule cell layer neurons (EGL), Internal granule cell layer and other neurons in the interior of the cerebellum (IGL), two clusters of Purkinje cell layer neurons (PCL), oligodendrocyte progenitor cells (OPCs), Atoh1+ neuronal progenitors, Ptf1a+ neuronal progenitors and other neuronal progenitors (NPCs) (C) In-situ hybridization images from the Allen Brain Atlas depicting expression of marker genes in specific layers. (D) Expression patterns of selected marker genes across cell types.\n\nC_FIG

molecular biology↗