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Hofmann, J.

Publications and source records attributed to Hofmann, J..

14 recordsLinked to original sources

Reducing transitory starch in cassava impairs photosynthesis and carbon export to storage roots

Optimizing source-sink relations is a central strategy for improving crop yield. In potato, reducing transitory leaf starch synthesis can redirect carbon to storage organs without impairing growth. To test whether this strategy is transferable to cassava, we suppressed the major small subunit of ADP-GLUCOSE PYROPHOSPHORYLASE, MeAPS1a. Transgenic plants were nearly devoid of transitory leaf starch and showed impaired photosynthetic carbon fixation. Under greenhouse conditions, shoots acclimated to the reduced carbon supply and exhibited only moderate biomass losses, and the data indicated reduced carbon supply to developing storage roots. This was reflected by lower leaf sucrose levels, reduced storage root biomass and starch accumulation, and downregulation of carbohydrate-responsive genes, including the major AGPase large subunit MeAPL3. Under field conditions, the absence of transitory starch was even more detrimental, causing severe growth inhibition and drastic reductions in both shoot and root biomass. We also found that MeAPS1a-derived small interfering RNAs moved systemically from leaves to roots, with lower root siRNA abundance in older, larger plants than in younger, smaller plants. Together, our results demonstrate that transitory starch is indispensable for sustaining carbon flux to cassava storage roots, highlighting species-specific constraints on engineering source-sink relations.

plant biology↗

Ex Vivo Assay for Organ-Specific Cancer Cell Invasion

BackgroundMetastasis is the leading cause of cancer-related mortality, yet experimental models often fail to recapitulate the tissue-specific microenvironments that shape metastatic dissemination. While in vivo systems provide physiological relevance, they are poorly suited for mechanistic studies. Conversely, conventional in vitro assays lack the organ-specific extracellular matrix (ECM) context that critically regulates invasive behavior. There is therefore a need for accessible models that balance biological relevance with experimental feasibility. ResultsIn this study, we developed an ex vivo invasion platform based on mild detergent decellularization of mouse organs followed by vibratome slicing. This approach generates optically transparent lung, liver, and intestine ECM scaffolds that preserve native matrix architecture, mechanical properties, and retain biochemical hallmarks of their tissues of origin. Organ-derived matrices were integrated into standard microfluidic channels and analyzed using conventional fluorescence microscopy to enable quantitative assessment of cancer cell invasion. Benchmarking with breast cancer cell lines of defined invasive capacity, we could demonstrate the robustness and biological relevance of the system. Non-invasive MCF7 cells failed to infiltrate any organ scaffold, whereas highly invasive MDA-MB-231 cells exhibited pronounced organ-specific invasion. These cells preferentially invaded lung and liver ECM while showing minimal invasion of intestinal scaffolds, recapitulating clinically observed metastatic tropism. Quantitative invasion rates closely matched values previously reported in vivo using intravital microscopy. ConclusionsThis ex vivo organ-derived ECM platform provides a scalable, cost-effective, and experimentally accessible system to study ECM-driven determinants of metastatic invasion. By preserving tissue-specific matrix cues while reducing reliance on animal models, this approach provides a powerful tool to interrogate ECM-driven determinants of metastasis and to evaluate potential therapeutic interventions.

cancer biology↗

Ischemic injury triggers a protective microglial phenotype in models of Aβ pathology

Microglia are highly plastic cells that are capable of integrating subsequent insults. As the majority of Alzheimers Disease (AD) patients also show cerebrovascular pathology, we here aimed to dissect the interactions between AD and ischemic brain injury on the microglial response to amyloid beta (A{beta}) pathology. Surprisingly, we find that ischemic stroke in the presence of cerebral {beta}-amyloidosis results in the generation of a novel neuroprotective microglial phenotype. These microglia drive a rapid accumulation of highly dense A{beta} plaques that exhibit a relatively benign nature and are strikingly similar to A{beta} plaques observed in patients that are resilient to AD pathology. Thus, our data do not only highlight the impact of a co-morbid state of brain ischemia and A{beta} pathology on the microglial phenotype but also identify novel molecular pathways that may serve to promote beneficial microglial functions in AD.

neuroscience↗

Tissue-resident neutrophils serve homeostatic and immunological functions in embryos

Development of neutrophils in the bone marrow and their crucial role in first-line defense are well understood in adults, but remarkably little is known about fetal neutrophils. Here, we analyzed the production, distribution, and functions of neutrophils during embryonic development in the mouse. We discovered that multiple non-hematopoietic steady-state organs harbor substantial numbers of immature and mature neutrophils, many of which are localized to tissue parenchyma outside the vessels. Using single-cell transcriptomic analyses, we revealed the presence of neutrophil progenitors and precursor cells in the blood and even in non-hematopoietic tissues in fetal and newborn mice. Embryonic tissue-resident neutrophils were transcriptionally different from embryonic blood-borne neutrophils and adult neutrophils. We demonstrated, through functional analyses, that embryonic neutrophils proliferated actively, had a high glycolytic capacity, and exhibited distinct diurnal rhythmicity. Embryonic neutrophils displayed lineage-specific innate immune effector functions and were responsive to maternal immunostimulation and immunosuppression. Using a genetic embryonic neutrophil depletion model, we discovered that neutrophils impact the piRNA pathway in the testis. Collectively, our data provides an atlas of the fetal neutrophil landscape and dissects their responses in steady-state. SummaryNon-hematopoietic steady-state tissues harbor extravascular immature and mature neutrophils during fetal development. Embryonic neutrophils are endowed with multiple effector mechanisms and also serve homeostatic roles during tissue development.

immunology↗

Predicting forest tree leaf phenology under climate change using satellite monitoring and population-based GWAS

Leaf phenology, a critical determinant of plant fitness and ecosystem function, is undergoing rapid shifts due to climate change, yet its complex genetic and environmental drivers remain incompletely understood. Understanding the genetic basis of phenological adaptation is crucial for forecasting forest responses to a changing climate. Here, we integrate multi-year satellite-derived phenology from 46 Fagus sylvatica (European beech) populations across Germany with a population-based genome-wide association study to dissect the environmental and genetic drivers of leaf-out day (LOD) and leaf shedding day (LSD). We show that environmental factors, particularly temperature forcing and water availability, are the primary drivers of LOD variation, while LSD is influenced by a more complex suite of climatic cues. Our genomic analysis identifies candidate genes associated with LOD and LSD, primarily linked to circadian rhythms and dormancy pathways, respectively. Furthermore, genomic prediction models incorporating these loci accurately reconstruct past phenological dynamics, providing a powerful framework to forecast forest vulnerability and adaptation to future climate change.

evolutionary biology↗

Mucosal innate immune activation as the trigger to Prevotella species-induced arthritis in genetically resistant mice

An altered gut microbiota, particularly the expansion of Prevotellaceae members, is increasingly implicated in the pathogenesis of rheumatoid arthritis (RA), yet the mechanisms hind this phenomenon remain unclear. Here, we demonstrate that Palleniella intestinalis, a member of the Prevotellaceae family, induces a 100% arthritis incidence in genetically resistant C57BL/6 mice. Inoculation with P. intestinalis modifies gut microbiota ecology, increases intestinal permeability, and selectively activates colonic CD11bCD11c myeloid cells, facilitating Th17 differentiation and driving joint inflammation. In vitro, outer membrane vesicles (OMV) from P. intestinalis and Segatella copri (formerly known as Prevotella copri) prime bone marrow-derived dendritic cells (BMDCs) to drive Th17 differentiation in an IL-6-dependent manner. Similar changes with increase in innate immune cell activation and IL-6 levels were shown in gut biopsies from new-onset RA patients. The transfer of Prevotellaceae-derived OMVs or Prevotellaeae-primed BMDCs replicates the hightened arthritis incidence in resistant mice, highlighting the critical role of intestinal immune activation in RA. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=130 SRC="FIGDIR/small/643707v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@1ce227corg.highwire.dtl.DTLVardef@3a2d0eorg.highwire.dtl.DTLVardef@16404b6org.highwire.dtl.DTLVardef@1717dc1_HPS_FORMAT_FIGEXP M_FIG C_FIG O_LIColonization with Paleniella intestinalis bypasses genetic resistance, consistently inducing arthritis incidence in non-susceptible C57BL/6 mice C_LIO_LIP. intestinalis activates colonic CD11b+CD11c+ myeloid cells, driving systemic Th17 cell differentiation C_LIO_LIIn vitro, outer membrane vesicles from P. intestinalis or RA-derived S. copri RPC01 primed DCs that drive Th17 differentiation in an IL-6-dependent manner C_LIO_LITransfer of P. intestinalis-primed DCs or its outer membrane vesicles alone increases arthritis incidence in non-susceptible C57BL/6 mice C_LI

immunology↗

Gut-specific H3R signaling orchestrates microglia-dependent resolution of peripheral inflammation

Chronic inflammatory diseases, like rheumatoid arthritis (RA) have been described to cause central nervous system (CNS) activation. Less is known about environmental factors that enable the CNS to suppress peripheral inflammation in RA. Here, we identified gut microbiota-derived histamine as such factor. We show that low levels of histamine activate the enteric nervous system, increase inhibitory neurotransmitter concentrations in the spinal cord and restore homeostatic microglia, thereby reducing inflammation in the joints. Selective histamine 3 receptor (H3R) signaling in the intestine is critical for this effect, as systemic and intrathecal application did not show effects. Microglia depletion or pharmacological silencing of local nerve fibers impaired oral H3R agonist-induced pro-resolving effects on arthritis. Moreover, therapeutic supplementation of the SCFA propionate identified one way to expand local intestinal histamine concentrations in mice and humans. Thus, we define a gut-CNS-joint axis pathway where microbiota-derived histamine initiates the resolution of arthritis via the CNS. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=109 HEIGHT=200 SRC="FIGDIR/small/603031v1_ufig1.gif" ALT="Figure 1"> View larger version (54K): org.highwire.dtl.DTLVardef@c217b8org.highwire.dtl.DTLVardef@a340ceorg.highwire.dtl.DTLVardef@1f3c1d8org.highwire.dtl.DTLVardef@3b6fc9_HPS_FORMAT_FIGEXP M_FIG C_FIG O_LIGut microbiota-derived histamine activates enteric neurons via H3R C_LIO_LILocal intestinal H3R activation induces shift to homeostatic microglia in the spinal cord C_LIO_LICNS controlled decrease in endothelial leakiness resolves synovial inflammation C_LI

immunology↗

B/T cell crosstalk and aberrant inflammatory IgG exacerbate autoimmune intestinal inflammation

Dysregulated B cell responses have been described in inflammatory-bowel disease (IBD) patients; however, the role of B cells in IBD pathology remained incompletely understood. We here described Wiskott-Aldrich Syndrome interacting protein deficient (Wipf1-/-) mice as novel mouse model of spontaneous, chronic colitis modelling human IBD. Concomitant with aberrant IgG production in colonic tissue of Wipf1-/- mice, we identified systemic, hypo-sialylated IgG as drivers of IL-1{beta} production in monocytes. Pathological antibody production was promoted by the hyper-reactivity of Wipf1-/- B cells in response to LPS stimulation, resulting in efficient activation of the MAPK/Erk and mTOR/Akt/4E-BP1 pathways and heightened metabolic activity. In addition to abundant inflammatory IgG, we found that B cells directly promoted the production of pro-inflammatory cytokines by intestinal CD4+ T cells. B/T co-culture assays defined the co-stimulatory molecule CD86 as driver of IFN-{gamma} and GM-CSF production by CD4+ T cells. CD86 expression was further enhanced by the presence of sCD40L, which was elevated in sera of Wipf1-/- mice. Similarly, colonic B cells of IBD patients expressed increased mRNA levels of CD86 correlating with enhanced levels of systemic sCD40L. Together, B cell-mediated pro-inflammatory cytokine secretion and B cell-derived inflammatory antibody production contributed to exacerbated pathogenesis during intestinal inflammation. O_FIG O_LINKSMALLFIG WIDTH=168 HEIGHT=200 SRC="FIGDIR/small/507066v1_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@1449ae8org.highwire.dtl.DTLVardef@116045borg.highwire.dtl.DTLVardef@77f3f2org.highwire.dtl.DTLVardef@130a271_HPS_FORMAT_FIGEXP M_FIG C_FIG One Sentence SummaryB cells fuel intestinal inflammation

immunology↗

Alcohol-sourced acetate reduces T cell filamentous actin branching and migration

Alcohol is among the most widely consumed dietary substances. Excessive alcohol consumption damages the liver, heart and brain. Alcohol also has strong immunoregulatory properties. Here we report how alcohol impairs T cell function via acetylation of cortactin, a protein that binds filamentous actin and facilitates branching. Upon alcohol consumption, acetate, the metabolite of alcohol, accumulates in lymphoid organs. T cells exposed to acetate, exhibit increased acetylation of cortactin. Acetylation of cortactin inhibits filamentous actin binding and hence reduces T cell migration, immune synapse formation and activation. While mutated, acetylation-resistant cortactin rescued the acetate-induced inhibition of T cell migration, primary mouse cortactin knock-out T cells exhibited impaired migration. Furthermore, acetate-induced cytoskeletal changes effectively inhibited activation, proliferation, and immune synapse formation in T cells in vitro and in vivo in an influenza infection model in mice. Together these findings reveal cortactin as a possible target for mitigation of T cell driven autoimmune diseases.

immunology↗

Assessment of binocular fixational eye movements including cyclotorsion with split-field binocular scanning laser ophthalmoscopy

Fixational eye movements are a hallmark of human gaze behavior, yet little is known about how they interact between fellow eyes. Here, we designed, built and validated a split-field binocular scanning laser ophthalmoscope (bSLO) to record high-resolution eye motion traces from both eyes of six observers during fixation at different binocular vergence conditions. In addition to microsaccades and drift, torsional eye motion could be extracted, with a spatial measurement error of less than 1 arcmin. Microsaccades were strongly coupled between fellow eyes under all conditions. No monocular microsaccade occurred and no significant delay between microsaccade onsets across fellow eyes could be detected. Cyclotorsion was also firmly coupled between both eyes, occurring typically in conjugacy, with gradual changes during drift and abrupt changes during saccades.

bioengineering↗

Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA

Integrity of mitochondrial DNA (mtDNA), encoding several subunits of the respiratory chain, is essential to maintain mitochondrial fitness. Mitochondria, as a central hub for metabolism, are affected in a wide variety of human diseases but also during normal ageing, where mtDNA integrity is compromised. Mitochondrial quality control mechanisms work at different levels, and mitophagy and its variants are critical to remove dysfunctional mitochondria together with mtDNA to maintain cellular homeostasis. Understanding the mechanisms governing a selective turnover of mutation-bearing mtDNA without affecting the entire mitochondrial pool is fundamental to design therapeutic strategies against mtDNA diseases and ageing. Here we show that mtDNA depletion after expressing a dominant negative version of the mitochondrial helicase Twinkle, or by chemical means, is due to an exacerbated mtDNA turnover. Targeting of nucleoids is controlled by Twinkle which, together with the mitochondrial transmembrane proteins ATAD3 and SAMM50, orchestrate mitochondrial membrane remodeling to form extrusions. mtDNA removal depends on autophagy and requires the vesicular trafficking protein VPS35 which binds to Twinkle-enriched mitochondrial subcompartments upon mtDNA damage. Stimulation of autophagy by rapamycin selectively removes mtDNA deletions which accumulated during muscle regeneration in vivo, but without affecting mtDNA copy number. With these results we unveil a new complex mechanism specifically targeting and removing mutant mtDNA which occurs outside the mitochondrial network. We reveal the molecular targets involved in a process with multiple potential benefits against human mtDNA related diseases, either inherited, acquired or due to normal ageing.

cell biology↗

High-throughput Interpretation of Killer-cell Immunoglobulin-like Receptor Short-read Sequencing Data with PING

The killer-cell immunoglobulin-like receptor (KIR) complex on chromosome 19 encodes receptors that modulate the activity of natural killer cells, and variation in these genes has been linked to infectious and autoimmune disease, as well as having bearing on pregnancy and transplant outcomes. The medical relevance and high variability of KIR genes makes short-read sequencing an attractive technology for interrogating the region, providing a high-throughput, high-fidelity sequencing method that is cost-effective. However, because this gene complex is characterized by extensive nucleotide polymorphism, structural variation including gene fusions and deletions, and a high level of homology between genes, its interrogation at high resolution has been thwarted by bioinformatic challenges, with most studies limited to examining presence or absence of specific genes. Here, we present the PING (Pushing Immunogenetics to the Next Generation) pipeline, which incorporates empirical data, novel alignment strategies and a custom alignment processing workflow to enable high-throughput KIR sequence analysis from short-read data. PING provides KIR gene copy number classification functionality for all KIR genes through use of a comprehensive alignment reference. The gene copy number determined per individual enables an innovative genotype determination workflow using genotype-matched references. Together, these methods address the challenges imposed by the structural complexity and overall homology of the KIR complex. To determine copy number and genotype determination accuracy, we applied PING to European and African validation cohorts and a synthetic dataset. PING demonstrated exceptional copy number determination performance across all datasets and robust genotype determination performance. Finally, an investigation into discordant genotypes for the synthetic dataset provides insight into misaligned reads, advancing our understanding in interpretation of short-read sequencing data in complex genomic regions. PING promises to support a new era of studies of KIR polymorphism, delivering high-resolution KIR genotypes that are highly accurate, enabling high-quality, high-throughput KIR genotyping for disease and population studies. Author summaryKiller cell immunoglobulin-like receptors (KIR) serve a critical role in regulating natural killer cell function. They are encoded by highly polymorphic genes within a complex genomic region that has proven difficult to interrogate owing to structural variation and extensive sequence homology. While methods for sequencing KIR genes have matured, there is a lack of bioinformatic support to accurately interpret KIR short-read sequencing data. The extensive structural variation of KIR, both the small-scale nucleotide insertions and deletions and the large-scale gene duplications and deletions, coupled with the extensive sequence similarity among KIR genes presents considerable challenges to bioinformatic analyses. PING addressed these issues through a highly-dynamic alignment workflow, which constructs individualized references that reflect the determined copy number and genotype makeup of a sample. This alignment workflow is enabled by a custom alignment processing pipeline, which scaffolds reads aligned to all reference sequences from the same gene into an overall gene alignment, enabling processing of these alignments as if a single reference sequence was used regardless of the number of sequences or of any insertions or deletions present in the component sequences. Together, these methods provide a novel and robust workflow for the accurate interpretation of KIR short-read sequencing data.

immunology↗

Mitochondrial function is essential for humoral immunity by controlling flux of the TCA cycle, phosphatidic acid and mTOR activity in B cells

The function of mitochondrial respiration during B cell fate decisions and differentiation remains equivocal. This study reveals that selection for mitochondrial fitness occurs during B cell activation and is essential for subsequent plasma cell differentiation. By expressing a mutated mitochondrial helicase in transitional B cells, we depleted mitochondrial DNA during B cell maturation, resulting in reduced oxidative phosphorylation. Although no changes in follicular B cell development were evident, germinal centers, class switch recombination to IgG, plasma cell generation and humoral immunity were diminished. Defective oxidative phosphorylation led to aberrant flux of the tricarboxylic acid cycle and lowered the amount of saturated phosphatidic acid. Consequently, MTOR activity and BLIMP-1 induction were curtailed whereas HIF1, glycolysis and AMPK activity were amplified. Exogenous phosphatidic acid increased mTOR activity in activated B cells. Hence, mitochondrial function is required and selected for in activated B cells for the successful generation of functional plasma cells.

immunology↗

PGP-UK: a research and citizen science hybrid project in support of personalized medicine

Molecular analyses such as whole-genome sequencing have become routine and are expected to be transformational for future healthcare and lifestyle decisions. Population-wide implementation of such analyses is, however, not without challenges, and multiple studies are ongoing to identify what these are and explore how they can be addressed. Defined as a research project, the Personal Genome Project UK (PGP-UK) is part of the global PGP network and focuses on open data sharing and citizen science to advance and accelerate personalized genomics and medicine. Here we report our findings on using an open consent recruitment protocol, active participant involvement, open access release of personal genome, methylome and transcriptome data and associated analyses, including 47 new variants predicted to affect gene function and innovative reports based on the analysis of genetic and epigenetic variants. For this pilot study, we recruited ten participants willing to actively engage as citizen scientists with the project. In addition, we introduce Genome Donation as a novel mechanism for openly sharing previously restricted data and discuss the first three donations received. Lastly, we present GenoME, a free, open-source educational app suitable for the lay public to allow exploration of personal genomes. Our findings demonstrate that citizen science-based approaches like PGP-UK have an important role to play in the public awareness, acceptance and implementation of genomics and personalized medicine.

genomics↗