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Biology subjects

Schumacher, J.

Publications and source records attributed to Schumacher, J..

At least 19 recordsLinked to original sources

AlphaVaR: an R framework for the statistical interpretation of AlphaGenome variant-effect predictions

SummaryAlphaGenome (Google DeepMind) scores a DNA variant across thousands of functional tracks at single-base resolution, reporting both the magnitude of each predicted effect and its rarity against a genome-wide background. That volume is itself the obstacle to biological interpretation. Here we present AlphaVaR, an R package that gives AlphaGenomes output a typed structure together with the statistical methods and visualizations needed to interpret it. The output schema is identical for every variant, so the same tests apply throughout it. AlphaVaR provides localization tests with multiple-testing correction and effect sizes, a specificity index measuring how far an effect concentrates on a few elements of a chosen variable, and a transparent prioritization that ranks candidates across interpretable criteria and maps each to a target gene. Results feed a plot library, reproducible reports and a code-free Shiny application. Applied to rs1427407, the lead common variant for fetal-haemoglobin level, AlphaVaR recovers the established biology of the BCL11A erythroid enhancer. Availability and implementationhttps://github.com/KarimMarhaba/AlphaVaR, released under the MIT licence, R [≥] 4.2, with documentation at https://karimmarhaba.github.io/AlphaVaR/. The released version is archived at Zenodo (doi:10.5281/zenodo.21939265); the AlphaGenome scores analysed here are archived as a separate dataset (doi:10.5281/zenodo.21920988), and the scripts that regenerate every figure and reported number are in the repository (Supplementary Section S5). Contactpouria.dasmeh@uni-marburg.de Supplementary informationSupplementary data are available online.

genomics↗

Biophysical properties of material-colonizing fungal biofilms: multiscale structural and mechanical characterization

Black extremotolerant fungi form persistent biofilms on a wide range of natural and engineered substrates. Able to weather minerals, affect stone monument surfaces, and colonize solar panels, they demonstrate a strong capacity to interact with and modify material surfaces, even under most extreme conditions. In this study, we establish a methodological workflow for the structural and mechanical characterization of melanized biofilms formed by the black fungus Knufia petricola. This species represents a broader group of resilient surface colonizers and provides a model for in-depth investigation. When grown on solid agar/air interface, this species predominantly forms a compact biofilm, composed of spherical cells, while retaining the capacity for filamentous growth, providing a suitable framework to explore morphology-dependent biomechanical responses. The proposed toolbox combines complementary analytical techniques spanning multiple spatial scales, including shear-rheology to quantify bulk viscoelastic behavior, micro-indentation to resolve local stiffness of the biofilm surface, micro-computed tomography for non-destructive three-dimensional visualization of biofilm architecture, and cryogenic preparation methods and electron microscopy for high-resolution ultrastructural analysis. As a case study, we applied this workflow to compare biofilms grown on two nitrogen sources (NO3- vs. NH4+). Our results reveal that the nitrogen source plays a key role in biofilm morphology across multiple hierarchical levels - ranging from cell division patterns and distribution of extracellular polymeric substances (EPS) to overall mechanical properties, where NO3- leads to budding-dominated growth and increased stiffness, whereas NH4+ promotes meristematic growth and softer biofilms. The successful transfer and integration of methods originally developed for bacterial biofilm research highlights the feasibility of quantitative mechanical analyses in fungal systems. This multiscale toolbox provides a foundation for advancing the mechanistic understanding of fungal biofilms and biofilm-material interactions, with implications for geomicrobiology, material biodeterioration, and the design of bio-inspired functional materials. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=147 SRC="FIGDIR/small/720134v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@7fd08borg.highwire.dtl.DTLVardef@15476c2org.highwire.dtl.DTLVardef@40be50org.highwire.dtl.DTLVardef@8e9410_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗

A host-directed virulence factor of Clostridium perfringens is modulated by gut commensal strains

In a healthy host, the residential microbes help regulate the growth of pathobionts, which are common members of the human gut microbiome, preventing them from causing diseases, including infections, under certain conditions. In cases of dysbiosis, this protection may be compromised. Targeted microbiome modulation offers a promising approach to restore healthy conditions in a disrupted community and consequently prevent infections using the natural colonization resistance of the microbiome. Elucidating the interaction mechanisms between microbial species within a microbiome is crucial for understanding how a microbiome can be modulated precisely and effectively to benefit the hosts well-being. Here, we investigated the interactions between the pathobiont C. perfringens and human gut commensals on physiological and molecular levels. We found that commensal strains affect C. perfringens growth by competing for substrates such as amino acids or a carbon source other than glucose. We further observed that Bacteroidaceae strains altered the levels of C. perfringens proteins, among others, the host-directed {theta}-toxin. Our findings reinforce the notion that modulating the composition of the gut microbiome is an effective strategy to prevent infections.

microbiology↗

Carbon and nitrogen availability affect biofilm growth and morphology of the extremotolerant fungus Knufia petricola

Rock-inhabiting fungi thrive in subaerial oligotrophic environments such as desert rocks, solar panels and marble monuments where organic carbon and nitrogen are scarce. We tested whether the rock-inhabiting fungus Knufia petricola showed a preference regarding nitrogen ([Formula] or [Formula]) and carbon (glucose or sucrose) sources and whether it was sensitive towards carbon and nitrogen limitation. As this fungus produces the carbon-rich, nitrogen-free 1,8-dihydroxynaphthalene (DHN) melanin, we tested whether a melanin-deficient mutant would be less sensitive to carbon limitation. The carbon and nitrogen concentrations were the primary predictors of growth, with a broad optimum partially explained by an optimal fungal C:N ratio. Limiting carbon or nitrogen supply decreased biomass formation, CO2 production and biofilm thickness but promoted substratum penetration through filamentous growth. The nitrogen content of the biomass was flexible within limits, increasing upon increasing nitrogen supply or decreasing carbon supply. The carbon use efficiency was fairly constant, whereas melanization correlated with a higher nitrogen content of the biomass despite melanin being nitrogen-free. In conclusion, in vitro, K. petricola switches to explorative growth under nutrient limitations, like fast-growing fungi, revealing universal fungal resource-acquisition patterns. Graphical abstract text and imageCarbon and nitrogen availability affect biofilm growth and morphology of the extremotolerant fungus Knufia petricola Abolfazl Dehkohneh, Julia Schumacher, Bastiaan J. R. Cockx, Karin Keil, Tessa Camenzind, Jan-Ulrich Kreft, Anna A. Gorbushina, Ruben Gerrits Growth of the rock-inhabiting fungus Knufia petricola was studied by varying carbon and nitrogen sources and concentrations. Overall, growth was best predicted by the carbon and nitrogen concentrations. Carbon and nitrogen limitation promoted substratum penetration through filamentous growth. O_FIG O_LINKSMALLFIG WIDTH=158 HEIGHT=200 SRC="FIGDIR/small/712823v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@6d98bdorg.highwire.dtl.DTLVardef@146aac5org.highwire.dtl.DTLVardef@757fa8org.highwire.dtl.DTLVardef@ff709_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

Iron acquisition strategies of the rock-inhabiting fungus Knufia petricola reveal vulnerability to chelator-based mitigation

Fungal iron acquisition has mostly been studied for pathogens living in competitive environments where securing iron from the host is critical for proliferation. How fungi from stress-rich but competition-free material surfaces handle iron uptake is, however, unknown. We studied these processes in rock-inhabiting fungi, known for their constitutive melanin-production, extremotolerant lifestyle and colonization of exposed surfaces such as solar panels and marble monuments, by choosing Knufia petricola to represent this group. The characterization of targeted mutants showed that K. petricola produces an extracellular - yet undefined - siderophore on which it relies less than on the ferroxidase-iron permease complex for reductive iron assimilation. By disrupting melanin synthesis, it was demonstrated that this pigment can reduce and adsorb iron but nevertheless does not contribute significantly to iron acquisition. Moreover, growth towards an iron source was found to be siderophore-dependent. Ferric citrate could not be directly assimilated. Finally, it was found that K. petricola and other rock-inhabiting fungi exhibited high sensitivity to strong iron chelators such as EDTA. These observations not only offer a potential mitigation strategy for preventing fungal colonization of subaerial materials using iron chelators, but also highlight the specialized adaptations of these fungi to low-competition environments. ImportanceThe rock-inhabiting fungus Knufia petricola acquires iron primarily via reductive iron assimilation, independently of the iron-adsorbing and -reducing melanin. Its siderophore, although extracellular and allowing chemotropism towards an iron source, is not able to obtain iron from strong iron chelators such as BPS and EDTA. This sensitivity to iron sequestration opens avenues to mitigate the fungal colonization of materials such as solar panels.

microbiology↗

Gene Interaction Network Architecture of Human Polygenic Traits Reveals Domain-Specific Connectivity and Evolutionary Pressures

Human polygenic phenotypes arise from complex interactions among genes within regulatory networks. To gain insights into the structural and evolutionary characteristics of these networks, we analyzed gene interaction networks across 4756 human polygenic phenotypes, contrasting the network properties of genes associated with polygenic phenotypes against those of non-associated genes. Our results indicate that genes associated with polygenic phenotypes exhibit a significantly higher connectivity in their corresponding gene-interaction networks, with connectivity varying markedly across different trait domains. Notably, genes within highly connected networks are enriched for immune-related biological processes, whereas genes in less connected networks are more involved in neurogenesis. Furthermore, we found that genes embedded in highly connected networks are, on average, under weaker selective constraints than those in lowly connected networks. Overall, our findings provide a systematic analysis of gene interaction networks underlying human polygenic traits and reveal how selective constraints vary with network connectivity. These insights offer a framework for prioritizing genes based on their connectivity within trait-associated networks. To support this effort, we developed the online portal http://netpolygen.com enabling researchers to generate and explore hypotheses by identifying genes that are both highly associated and highly connected across thousands of polygenic phenotypes.

evolutionary biology↗

Adaptation of Plasmid-ID Technology for Evaluation of N2-Fixing Effectiveness and Competitiveness for Root Nodulation in the Sinorhizobium-Medicago System

Maximizing the nitrogen fixation occurring in rhizobia-legume associations represents an opportunity to sustainably reduce nitrogen fertilizer inputs in agriculture. High-throughput measurement of symbiotic traits has the potential to accelerate the identification of elite rhizobium/legume associations and enable novel research approaches. Plasmid-ID technology, recently deployed in Rhizobium leguminosarum, facilitates the concurrent assessment of rhizobium nitrogen-fixing effectiveness and competitiveness for root nodulation. This study adapts Plasmid-ID technology to function in Sinorhizobium species that are central models for studying rhizobium-legume associations and form economically important symbioses with alfalfa. New Sino-Plasmid-IDs were developed and tested for stability and their ability to measure competitiveness for root nodulation and nitrogen-fixing effectiveness. Rhizobial competitiveness is measured by identifying strain-specific nucleotide barcodes using Next-Generation Sequencing while effectiveness is measured by GFP fluorescence driven by the synthetic nifH promoter. Sino-Plasmid-IDs allow researchers to efficiently study competitiveness and effectiveness in a multitude of Sinorhizobium strains simultaneously.

microbiology↗

BEVA2.0: Modular Assembly of Golden Gate-Compatible Vectors with Expanded Utility for Genetic Engineering

This expansion for the modular vector assembly platform BEVA (Bacterial Expression Vector Archive) introduces 11 new BEVA parts including two new cloning site variants, two new antibiotic resistance modules, three new origins of replication, and four new accessary modules. As a result, the modular system is now doubled in size and expanded in its capacity to produce diverse replicating plasmids. Furthermore, it is now amenable to genetic engineering methods involving genome-manipulation of target strains through deletions or integrations. In addition to introducing the new modules, we provide several BEVA-derived Golden Gate cloning plasmids that are used to validate parts and that may be useful for genetic engineering of proteobacteria and other bacteria. We also introduce new parts to allow compatibility with the CIDAR MoClo parts libraries.

synthetic biology↗

Single cell analysis of Barrett's esophagus and carcinoma reveals cell types conferring risk via genetic predisposition

Inherited genetic variants contribute to Barretts esophagus (BE) and esophageal adenocarcinoma (EAC) but it is unknown which cell types are involved in this process. We performed single cell RNA-sequencing of BE, EAC and paired normal tissues and integrated data of a genome-wide association study to determine cell type-specific genetic risk and cellular processes that contribute to BE and EAC. The analysis revealed that EAC development is driven to a greater extent by local cellular processes than BE development. One cell type of BE origin (BE-EAC) and cellular processes that control the differentiation of columnar cells are of particular relevance for EAC development. Further, specific subtypes of fibroblasts and endothelial cells contribute to BE and EAC development, while dendritic cells and CD4+ memory T cells contribute exclusively to BE development. The diagnostic use of markers characterizing the identified cell types and cellular processes should be explored in future for EAC prediction.

cancer biology↗

Proton-pump inhibitors increase C. difficile infection risk by altering pH rather than by affecting the gut microbiome based on a bioreactor model

Clostridioides difficile infections often occur after antibiotic use, but they have also been linked to proton-pump inhibitor (PPI) therapy. The underlying mechanism--whether infection risk is due to a direct effect of PPIs on the gut microbiome or changes in gastrointestinal pH--has remained unclear. To disentangle both possibilities, we studied the impact of the proton-pump inhibitor omeprazole and pH changes on key members of the human gut microbiome and stool-derived microbial communities from different donors in vitro. We then developed a custom multiple-bioreactor system to grow a model human microbiome community in chemostat mode and tested the effects of omeprazole exposure, pH changes, and their combination on C. difficile growth within this community. Our findings show that changes in pH significantly affect the gut microbial communitys biomass and the abundances of different strains, leading to increased C. difficile growth within the community. However, omeprazole treatment alone did not result in such effects. These findings imply that the higher risk of C. difficile infection following proton-pump inhibitor therapy is probably because of alterations in gastrointestinal pH rather than a direct interaction between the drug and the microbiome. This understanding paves the way for reducing infection risks in proton-pump inhibitor therapy.

microbiology↗

Nerve injury converts Schwann cells in a persisting repair state in human neuroma tissue

Peripheral nerve injury (PNI) induces neuroma formation at the severed nerve stump resulting in impaired nerve regeneration and functional recovery in patients. So far, molecular mechanisms and cell types present in the neuroma impeding on regeneration have only sparsely been analyzed. Herein we compare resected human neuroma tissue with intact donor nerves from the same patient. Neuroma from several post-injury timepoints (1-13 months) were included, thereby allowing for temporal correlation with molecular and cellular processes. We observed reduced axonal area and percentage of myelin producing Schwann cells (SCs) compared to intact nerves. However, total SOX10 positive SC numbers were comparable. Notably, markers for SCs in a repair mode including c-JUN and SHH (sonic hedgehog) and SC proliferation (pH3) were upregulated in neuroma, suggesting presence of SCs in repair rather than differentiated status. In agreement, in neuroma, pro-regenerative markers such as phosphorylated i.e. activated CREB (pCREB), ATF3, GAP43 and SCG10 were upregulated. Neuroma tissue was infiltrated by several types of macrophages. Finally, when taken in culture, neuroma SCs were indistinguishable from controls SCs with regard to proliferation and morphology. However, cultured neuroma SCs retained a different molecular signature from control SCs including increased inflammation and reduced gene expression for differentiation markers such as myelin genes. In summary, human neuroma tissue consists of SCs with a repair status and is infiltrated strongly by several types of macrophages.

neuroscience↗

Human Th17- and IgG3-associated autoimmunity induced by a translocating gut pathobiont

Extraintestinal autoimmune diseases are multifactorial with translocating gut pathobionts implicated as instigators and perpetuators in mice. However, the microbial contributions to autoimmunity in humans remain largely unclear, including whether specific pathological human adaptive immune responses are triggered by such pathobionts. We show here that the translocating pathobiont Enterococcus gallinarum induces human IFN{gamma}+ Th17 differentiation and IgG3 subclass switch of anti-E. gallinarum RNA and correlating anti-human RNA autoantibody responses in patients with systemic lupus erythematosus and autoimmune hepatitis. Human Th17 induction by E. gallinarum is cell-contact dependent and involves TLR8-mediated human monocyte activation. In murine gnotobiotic lupus models, E. gallinarum translocation triggers IgG3 anti-RNA autoantibody titers that correlate with renal autoimmune pathophysiology and with disease activity in patients. Overall, we define cellular mechanisms of how a translocating pathobiont induces human T- and B-cell-dependent autoimmune responses, providing a framework for developing host- and microbiota-derived biomarkers and targeted therapies in extraintestinal autoimmune diseases. One Sentence SummaryTranslocating pathobiont Enterococcus gallinarum promotes human Th17 and IgG3 autoantibody responses linked to disease activity in autoimmune patients.

immunology↗

Acute kidney injury-induced circulating TNFR1/2 elevations correlate with persistent kidney injury and progression to fibrosis

BackgroundElevated levels of circulating Tumor-Necrosis-Factor-Receptors 1 and 2 (cTNFR1/2) predict CKD progression. Whether acute kidney injury drives cTNFR1/2 elevations and whether they predict disease outcomes after AKI remains unknown. MethodsWe used AKI patient serum and urine samples, mouse models of kidney injury (ischemic, obstructive, toxic) and progression to fibrosis, nephrectomy, and related single cell RNA-sequencing datasets. ResultsWe show that TNFR1/2 serum and urine levels are highly elevated in all mouse models of kidney injury tested, beginning within one-hour post-injury, and correlate with its severity. Consistent with this, serum and urine TNFR1/2 levels are increased in AKI patients and correlate with severity of kidney failure. Interestingly, the extracellular vesicle (EV)-bound forms of cTNFR1/2 correlate with renal function better than their soluble forms. TNF neutralization does not affect early cTNFR1/2 elevations, suggesting that cTNFR1/2 levels do not reflect injury-induced TNF activity. Kidney tissue expression of TNFR1/2 after AKI is only mildly increased and bilateral nephrectomies lead to strong cTNFR1/2 elevations, suggesting release of these receptors by extrarenal sources. cTNFR1/2 remain elevated for weeks after severe kidney injury and at these later timepoints cTNFR1/2 correlate to remaining kidney injury. During AKI-to-CKD transition, kidney expression of TNFR1/2 and cTNFR2 levels, correlate with development of fibrosis. ConclusionsOur data demonstrate that AKI drives acute increases in cTNFR1/2 serum levels which negatively correlate with kidney function, in particular their EV-bound forms. Sustained TNFR1/2 elevations after kidney injury during AKI-to-CKD transition correlate with persistent tissue injury and progression to kidney fibrosis. Significance StatementCirculating TNF-Receptor-1 and -2 (cTNFR1/2) elevations predict chronic kidney disease progression. It remains unknown whether kidney injury can drive cTNFR1/2 elevations, whether cTNFR1/2 levels predict disease outcomes after AKI, and which are their circulating molecular forms. This study shows that kidney injury strongly increases cTNFR1/2 levels and that their extracellular vesicle-bound forms better correlate with kidney function loss, compared to their soluble forms. Sustained cTNFR1/2 elevations correlate to remaining kidney injury, and cTNFR1/2 levels post injury predict progression to kidney fibrosis. This work, thus, points to novel mechanisms for the observed cTNFR1/2 elevations in kidney disease and identifies unique predictive and diagnostic value in cTNFR1/2 elevations in AKI or AKI-to-CKD transition.

physiology↗

Arabidopsis thaliana BBX14 is a target of GLK1 and involved in high-light acclimation, photomorphogenesis and GUN-type retrograde signaling

Development of photosynthetically competent seedlings requires both light and retrograde biogenic signaling pathways. The transcription factor GLK1 functions at the interface between these pathways, and receives input from the biogenic-signaling integrator GUN1. BBX14 was previously identified, together with GLK1, in a core module that mediates the response to high light levels and biogenic signaling. To gain insight into the function of BBX14, we generated BBX14 overexpressors and CRISPR/Cas-mediated bbx14 mutant plants, conducted high-light, RT-qPCR and ChIP-Seq experiments, measured photosynthetic parameters, chlorophyll contents and growth rates, and analyzed alterations in transcriptomics. We found that, although overexpression of BBX14 is deleterious under normal growth conditions, BBX14 is needed to acclimate plants to high light stress. BBX14 is a direct target of GLK1, and RNA-Seq analysis suggests that BBX14 is involved in the circadian clock. Knockout of BBX14 results in a long-hypocotyl phenotype that depends on a retrograde signal, and BBX14 expression during biogenic signaling requires GUN1. Finally, we clarify the role of BBX14 in GUN-type biogenic signaling. We conclude that BBX14 is an integrator of photomorphogenetic and biogenic signals, and suggest that BBX14 is a nuclear target of retrograde signals downstream of the GUN1/GLK1 module.

plant biology↗

The first archaeal PET-degrading enzyme belongs to the feruloyl-esterase family

Polyethylene terephthalate (PET) is a commodity polymer known to globally contaminate marine and terrestrial environments. Today, around 40 bacterial and fungal PET-active enzymes (PETases) are known, originating from four bacterial and two fungal phyla. In contrast, no archaeal enzyme has been identified to degrade PET. Here we report on the structural and biochemical characterization of PET46, an archaeal promiscuous feruloyl esterase exhibiting degradation activitiy on PET, bis-, and mono-(2-hydroxyethyl) terephthalate (BHET and MHET). The enzyme, found by a sequence-based metagenome search, was derived from a non-cultivated, deep-sea Candidatus Bathyarchaeota archaeon. Biochemical characterization demonstrated that PET46 is a promiscuous, heat-adapted hydrolase. Its crystal structure was solved at a resolution of 1.71 [A]. It shares the core alpha/beta-hydrolase fold with bacterial PETases, but contains a unique lid common in feruloyl esterases, which is involved in substrate binding. Thus, our study significantly widens the currently known diversity of PET-hydrolyzing enzymes, by demonstrating PET depolymerization by a lignin-degrading esterase.

biochemistry↗

INSULIN-LIKE GROWTH FACTOR I REDUCES CORONARY ATHEROSCLEROSIS IN PIGS WITH FAMILIAL HYPERCHOLESTEROLEMIA

ObjectiveAlthough murine models of coronary atherosclerotic disease (CAD) have been used extensively to determine mechanisms, limited new therapeutic options have emerged. Pigs with familial hypercholesterolemia (FH pigs) develop complex coronary atheromas that are almost identical to human lesions. We reported previously that insulin-like growth factor 1 (IGF-1) reduced aortic atherosclerosis and promoted features of stable plaque in a murine model. We tested IGF-1 effects in atherosclerotic FH pigs to consider use of IGF-1 to treat CAD in humans. FH pigs were administered with IGF-1 for 6 months. Atherosclerosis was quantified by serial intravascular ultrasound (IVUS) and histology, plaque composition - by immunohistochemistry. We used spatial transcriptomics (ST) analysis to identify global transcriptome changes in advanced plaque compartments and to obtain mechanistic insights into IGF-1 effects. ResultsIGF-1-injected FH pigs had 1.8-fold increase in total circulating IGF-1 levels compared to control. IGF-1 decreased relative coronary atheroma (IVUS) and lesion cross-sectional area (histology). IGF-1 induced vascular hypertrophy and reduced circulating triglycerides, markers of systemic oxidative stress and pro-atherogenic CXCL12 chemokine levels. IGF-1 increased fibrous cap thickness, and reduced necrotic core size, macrophage content, and cell apoptosis, changes consistent with promotion of a stable plaque phenotype. IGF-1 suppressed FOS/FOSB factors and gene expression of MMP9 and CXCL14 in plaque macrophages, suggesting possible involvement of these molecules in IGF-1s effect on atherosclerosis. ConclusionsIGF-1 reduced coronary plaque burden and promoted features of stable plaque in a pig model, providing support for consideration of clinical trials. ST profiling of plaques provided novel insights into potential mechanisms.

cell biology↗

Diversity-induced plant history and soil history effects modulate plant responses to global change

Global change has dramatic impacts on grassland diversity. However, little is known about how fast species can adapt to these changes and how this affects their responses to global change. To close this gap, we performed a common garden experiment testing whether plant responses to global change are influenced by the selection history of the plants and the conditioning history of soil at different levels of plant diversity. Therefore, we collected seeds and took soil samples from 14-year old plant communities of a biodiversity experiment. Offspring of plants from low- and high-diversity communities were either grown in their own soil or in soil of a different community, and were either exposed to drought, increased nitrogen input, or a combination of both. Results show that, under nitrogen addition, offspring of plants selected at high diversity produced more biomass than those selected at low diversity, while drought neutralized differences in biomass production. Moreover, under the influence of global change drivers, mainly soil, and to a lesser extent plant history, influenced the expression of plant traits. Our results show that plant diversity modulates plant-soil interactions and growth strategies of plants, which feedback on the eco-evolutionary pathways of the plants and thus their responses to global change.

ecology↗

A 3D gene expression atlas of the floral meristem based on spatial reconstruction of single nucleus RNA sequencing data

Identity and functions of plant cells are influenced by their precise cellular location within the plant body. Cellular heterogeneity in growth and differentiation trajectories results in organ patterning. Therefore, assessing this heterogeneity at molecular scale is a major question in developmental biology. Single-cell transcriptomics (scRNA-seq) allows to characterize and quantify gene expression heterogeneity in developing organs at unprecedented resolution. However, the original physical location of the cell is lost during the scRNA-seq procedure. To recover the original location of cells is essential to link gene activity with cellular function and morphology. Here, we reconstruct genome-wide gene expression patterns of individual cells in a floral meristem by combining single-nuclei RNA-seq with 3D spatial reconstruction. By this, gene expression differences among meristematic domains giving rise to different tissue and organ types can be determined. As a proof of principle, the data are used to trace the initiation of vascular identity within the floral meristem. Our work demonstrates the power of spatially reconstructed single cell transcriptome atlases to understand plant morphogenesis. The floral meristem 3D gene expression atlas can be accessed at http://threed-flower-meristem.herokuapp.com

plant biology↗