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Geiss, C.

Publications and source records attributed to Geiss, C..

9 recordsLinked to original sources

Development of a multi-organ single-cell atlas of systemic sclerosis reveals shared and tissue-specific pathogenic pathways.

Objectives: Systemic sclerosis (SSc) is a multi-organ autoimmune disease for which no broadly effective disease-modifying treatment exists. We developed an integrated multi-organ single-cell atlas of SSc to identify shared and organ specific disease-associated transcriptional programmes and potential therapeutic targets. Methods: We integrated single-cell RNA-sequencing data from skin, lung, synovium, and peripheral blood mononuclear cells (six studies, 401,902 cells, 90 individuals) using Harmony. Pseudobulk differential expression and gene set enrichment analysis were performed at the tissue cell-compartment, cell-type, and subpopulation levels, including independent reclustering of lymphoid, myeloid and fibroblast populations. Results: Disease-associated transcriptional programmes showed marked tissue dependence, even within the same cell lineage, highlighting the importance of organ-specific mechanisms in SSc. Nevertheless, recurrent extracellular matrix (ECM) remodelling programmes were identified in lung, skin and synovium, and interferon signalling programmes in skin, synovium and peripheral blood mononuclear cells, across immune and fibroblast cell populations. Although no subpopulation was exclusive to SSc, a shared myofibroblast subpopulation expressing SFRP2, COL1A1, POSTN, ACTA2, and COMP was identified across lung, skin, and synovium. In addition, perivascular and mitotic fibroblast subpopulations exhibited both profibrotic and inflammatory signatures, including interferon- and IL-2-related signalling programmes. Conclusions: SSc is characterised by two complementary axes: a tissue-dependent cellular programme and a recurrent fibrotic and interferon-associated signature extending across multiple organs and cell populations. These findings are consistent with current organ-based therapeutic approaches while highlighting interferon signalling as a potential multi-organ therapeutic target. The resulting interactive single-cell atlas provides a resource for investigating shared and organ-specific disease mechanisms and guiding future therapeutic research.

immunology↗

Synovitis in systemic sclerosis is an interferon-driven stromal condition distinct from rheumatoid arthritis

Joint involvement is a major driver of disability in systemic sclerosis (SSc), yet its pathophysiology remains poorly understood. In the absence of specific evidence, SSc synovitis is treated by analogy with rheumatoid arthritis (RA). Here, we present the first comprehensive molecular characterization of SSc synovitis, integrating histology, single-cell RNA sequencing, and spatial multi-omics of synovial biopsies from SSc patients, RA patients, and non-inflammatory controls with in vitro validation. We show that SSc synovitis is characterized by distinct pathomechanisms from RA. Histologically, most SSc biopsies displayed a pauci-immune pathotype with sparse immune infiltrates and predominant stromal cells. At molecular level, synovial fibroblasts in SSc were characterized by a disease-specific type I interferon (IFN) response program, in contrast to the TNF-dominant profile of RA, accompanied by dysregulation of the complement cascade. This IFN program extended across multiple synovial cell types, including monocyte-derived macrophages and endothelial cells, and was spatially organized into focal myeloid niches and a diffuse stromal program. Systemically, elevated serum IFN-2a levels were associated with the presence of clinical synovitis in an independent cohort of SSc patients. We furthermore show that similar IFN-driven programs are shared between skin and synovium in SSc. Genes downregulated by IFNAR1 blockade in SSc skin were enriched in SSc synovium, supporting IFN receptor blockade as a multi-organ target therapeutic strategy. These findings reframe SSc synovitis as a less destructive, IFN-driven stromal condition distinct from RA and provide a mechanistic basis for dedicated clinical trials for joint inflammation in SSc. One Sentence SummarySSc synovitis is a pauci-immune, IFN-driven stromal condition distinct from RA, supporting IFNAR1 blockade as a therapeutic strategy. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=110 SRC="FIGDIR/small/733140v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@d85bb5org.highwire.dtl.DTLVardef@6cffe6org.highwire.dtl.DTLVardef@148eb4org.highwire.dtl.DTLVardef@1a4cd83_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Disease-specific fibroblast-myeloid interactions in rheumatoid arthritis synovium

Rheumatoid arthritis (RA) is characterized by profound remodeling of the synovial microenvironment. Here we show that enhanced fibroblast-macrophage cross-talk distinguishes RA from psoriatic arthritis (PsA). MerTK-SPP1 macrophages represent the dominant inflammatory myeloid population in RA, interacting with expanded fibroblast subsets through SPP1-mediated signaling. Lining fibroblasts display induction of antigen-presentation and IL-6/JAK-STAT pathways, while a CHI3L1-producing fibroblast population arises specifically in RA and may act as a source of autoantigens. These stromal populations interact closely with FABP5 iDC3 cells and T cells within a disrupted synovial lining, creating a niche driving adaptive immune activation. In contrast, PsA exhibits increased fibroblast- endothelial interactions without major endothelial transcriptional changes. Our data identify SPP1 signaling and fibroblast-myeloid-dendritic interactions as core drivers of RA synovial inflammation that links innate immune activation to the initiation of autoimmunity. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=78 SRC="FIGDIR/small/688477v1_ufig1.gif" ALT="Figure 1"> View larger version (25K): org.highwire.dtl.DTLVardef@c76e39org.highwire.dtl.DTLVardef@11563a9org.highwire.dtl.DTLVardef@141f3fborg.highwire.dtl.DTLVardef@f90742_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Decoding the functional role of the calcium ATPase YloB in microbially induced calcite precipitation and sporulation in Solibacillus silvestris

Calcium homeostasis is essential for bacterial physiology, yet its regulation and role in specialized processes such as microbially induced calcite precipitation (MICP) and sporulation remain poorly understood. Here, we characterized the sole annotated P-type calcium ATPase in Solibacillus silvestris, which was previously shown to be upregulated under MICP conditions. We named the protein YloB based on homology to the Bacillus subtilis protein. Structural modeling confirmed that YloB possesses the conserved domains and motifs typical of calcium binding P-type ATPases. Deletion of yloB did not affect growth under elevated calcium levels nor did it reduce MICP yields, indicating that YloB is dispensable for calcium detoxification and biomineralization. In contrast, {Delta}yloB cells produced only partially dehydrated spores with severely reduced heat resistance, a defect rescued by complementation. A YloB-mNeonGreen fluorescent fusion localized specifically to the cell membrane surrounding the forespore during early engulfment, and was retained at this site throughout the remainder of sporulation. A transcriptional PyloB-msfGFP reporter demonstrated that yloB transcription was induced in the early stages of sporulation, but did not respond to a calcium stimulus. These results show that YloB does not act to detoxify calcium from the cytoplasm of S. silvestris, but rather functions to pump calcium into the forespore, enabling Ca-dipicolinic acid accumulation and proper spore maturation. Our study reveals a specialized role for a bacterial calcium ATPase in sporulation, distinguishing calcium transport for endospore development from biomineralization and global calcium homeostasis.

microbiology↗

A bistable circuit regulates miRNA-155 levels in human macrophage inflammatory transitions

Macrophages are crucial immune regulators as they can either trigger or resolve inflammation. These properties rely on defined inflammatory states and make macrophages valuable therapeutic targets. Identification of stable steady states and bistability in inflammatory transitions provides deeper insights into immune regulation and facilitates the development of novel therapeutic strategies. We present a multiomic and systems biology approach for the top-down identification of bistable circuits in human macrophages polarized towards pro- and anti-inflammatory phenotypes. Using differential gene expression profiles, we identified three criteria to suspect bistability: two potential attractors, a hysteresis behavior between their transitions, and the presence of potential modules of coregulated genes. This was further confirmed by proteomics data pointing to mutually exclusive and time-dependent profiles of gene expression. By network simplification and creation of a novel pipeline for parameter estimation in bistable models, we obtained a minimal model of inflammatory transitions in which we identified ultrasensitivity and hysteresis. Our minimal model genes establish a regulatory circuit switching miR-155 expression, which in turn regulates the expression of inflammatory marker genes during inflammatory transitions.

systems biology↗

Assessment of technical and clinical utility of a bead-based flow cytometry platform for multiparametric phenotyping of CNS-derived extracellular vesicles

Extracellular vesicles (EVs) derived from the CNS are potential liquid-biopsy markers for early detection and monitoring of neurodegenerative diseases and brain tumors. This study assessed the performance of a bead-based flow cytometry assay (EV Neuro) for multiparametric detection of CNS-derived EVs and identification of disease-specific markers. Different sample materials and EV isolation methods were compared. Glioblastoma- and primary human astrocyte-derived EVs exhibited distinct EV profiles, with signal intensities increasing with higher EV input. Analysis of serum or plasma from glioblastoma, multiple sclerosis, Alzheimers Disease patients and healthy controls showed varying marker signal intensities. Notably, data normalization improved marker identification. Specific EV populations, such as CD36+EVs in glioblastoma and GALC+EVs in multiple sclerosis, were significantly elevated in disease compared to controls. Clustering analysis techniques effectively differentiated glioblastoma patients from controls. A potential correlation between CD107a+EVs and neurofilament levels in the blood was identified in multiple sclerosis patients. Together, the semi-quantitative EV Neuro assay demonstrated its utility for EV profiling in complex samples. However, reliable statistical results in biomarker studies require large sample cohorts and high effect sizes. Nonetheless, this exploratory trial confirmed the feasibility of discovering EV-associated biomarkers and monitoring circulating EV profiles in CNS diseases using the EV Neuro assay.

neuroscience↗

decoupleR: Ensemble of computational methods to infer biological activities from omics data

SummaryMany methods allow us to extract biological activities from omics data using information from prior knowledge resources, reducing the dimensionality for increased statistical power and better interpretability. Here, we present decoupleR, a Bioconductor package containing computational methods to extract these activities within a unified framework. decoupleR allows us to flexibly run any method with a given resource, including methods that leverage mode of regulation and weights of interactions. Using decoupleR, we evaluated the performance of methods on transcriptomic and phospho-proteomic perturbation experiments. Our findings suggest that simple linear models and the consensus score across methods perform better than other methods at predicting perturbed regulators. Availability and ImplementationdecoupleR is open source available in Bioconductor (https://www.bioconductor.org/packages/release/bioc/html/decoupleR.html). The code to reproduce the results is in Github (https://github.com/saezlab/decoupleR_manuscript) and the data in Zenodo (https://zenodo.org/record/5645208). ContactJulio Saez-Rodriguez at pub.saez@uni-heidelberg.de.

bioinformatics↗

MYC dosage compensation is mediated by miRNA-transcription factor interactions in aneuploid cancer

We hypothesize that dosage compensation of critical genes arises from systems-level properties for cancer cells to withstand the negative effects of aneuploidy. We identified several candidate genes in cancer multi-omics data and developed a biocomputational platform to construct a mathematical model of their interaction network with miRNAs and transcription factors, where the property of dosage compensation emerged for MYC and was dependent on the kinetic parameters of its feedback interactions with three micro-RNAs. These circuits were experimentally validated with a novel genetic tug-of-war technique by overexpressing an exogenous MYC leading to over-expression of the three microRNAs involved and down-regulation of endogenous MYC. In addition, MYC overexpression or inhibition of its compensating miRNAs led to dosage-dependent cytotoxicity in MYC-amplified colon cancer cells. Finally, we identified negative correlation of MYC dosage compensation with patient survival in TCGA breast cancer patients, highlighting the potential of this mechanism to prevent aneuploid cancer progression. HighlightsThe systems-level property of gene dosage-compensation emerges in silico in miRNA-transcription factor networks depending on the kinetic parameters of its interactions. We established a criterion to identify compensated candidate genes with low variation in expression despite high copy number variation. BioNetUCR is a novel biocomputational platform to model miRNA-transcription factor interactions We present a novel genetic tug-of-war technique to experimentally validate gene dosage compensation at the transcriptional level. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=131 SRC="FIGDIR/small/440572v2_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@104a93forg.highwire.dtl.DTLVardef@1039ae9org.highwire.dtl.DTLVardef@1af41c6org.highwire.dtl.DTLVardef@1073e6a_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

An F-actin shell ruptures the nuclear envelope by sorting pore-dense and pore-free membranes in meiosis of starfish oocytes

The nucleus of oocytes, traditionally referred to as the germinal vesicle, is unusually large and its nuclear envelope (NE) is densely packed with nuclear pore complexes (NPCs) stockpiled for embryonic development. We have shown that breakdown of this specialized NE during meiosis of starfish oocytes is mediated by an Arp2/3-nucleated F-actin shell, in contrast to microtubule-driven tearing in somatic cells. The detailed mechanism of how the cytoskeletal forces disrupt the NE remains poorly understood in any system. Here, we address the mechanism of F-actin-driven NE rupture by using live-cell and correlated super-resolution light and electron microscopy. We show that actin is nucleated within the lamina and sprouts filopodia-like spikes towards the nuclear membranes forcing lamina and nuclear membranes apart. These F-actin spikes protrude pore-free nuclear membranes, whereas the adjoining membrane stretches accumulate packed NPCs associated with the still-intact lamin network. NPC conglomerates sort into a distinct tubular-vesicular membrane network, while breaks appear in pore-free, ER-like regions. Together, our work reveals a novel function for Arp2/3-mediated membrane shaping in NE rupture that is likely to have broad relevance in regulating NE dynamics in diverse other contexts such as nuclear rupture frequently observed in cancer cells.

cell biology↗