bioRxiv Science⌕ Search

Biology subjects

Weiner, J.

Publications and source records attributed to Weiner, J..

14 recordsLinked to original sources

Recruitment of the local GABAergic population engages complex network interactions in the ventral subiculum

The ventral subiculum (vSub), a major output node of the hippocampal formation, has been implicated in diverse neurological disorders. Disruption of excitatory-inhibitory balance is a common feature of neurological disorders, with altered GABAergic signaling representing a critical component. More recently, the vSub has gained increasing attention as a component of neural circuits underlying emotional and motivational regulation, through its extensive connections with regions implicated in mental health disorders such as addiction and anxiety. Our previous work in models of alcohol use disorder and comorbid anxiety identified an important role for GABAergic inhibition in regulating vSub excitability, prompting us to investigate the functional consequences of recruiting the broader local GABAergic population. Although previous studies have examined individual interneuron subtypes, the network consequences of activating the global population of local GABAergic neurons remain poorly understood. To address this question, we expressed channelrhodopsin using an mDlx-dependent strategy to target GABAergic neurons in the ventral hippocampus and performed in vivo electrophysiological recordings from vSub neurons in anesthetized rats. Repeated activation of this GABAergic population at 20 Hz, a stimulation frequency commonly used in behavioral optogenetic studies, produced robust suppression of pyramidal neuron firing during stimulation. This direct inhibition was accompanied by network-dependent increases in post-stimulus activity that varied as a function of baseline activity, sex, and trial number. Complementary ex vivo electrophysiological experiments further supported network-dependent effects and revealed short-term synaptic plasticity that evolved across repeated stimulation trials, reflecting contributions from both pre- and postsynaptic mechanisms. Together, these findings demonstrate that recruitment of the broader GABAergic population produces effects extending beyond direct inhibition and can engage dynamic network responses that depend on stimulation history and circuit state. These findings highlight the importance of stimulation frequency, timing, and network context when interpreting the functional consequences of GABAergic circuit manipulation.

neuroscience↗

Kiosc: an integrated platform for managing bioinformatics data analysis containers

In many bioinformatic data analysis projects, it is convenient to visualize plots and results through an interactive web app or dashboard. These interactive reports can then be shared with customers, collaborators, or the general public. Publishing and sharing these apps is not straightforward, becoming especially cumbersome when the number of projects and customers start growing. Docker containers offer a convenient way to package, distribute, and run interactive web apps, and their use is already widespread in the bioinformatics community. We developed Kiosc to simplify the orchestration of containerized web apps, organize them into projects, and regulate access control. We implemented it as a web server based on the Django framework, with a user- and admin-friendly interface as well as a REST API for programmatic tasks. Users can select Docker containers packaging apps like Plotly Dash, Shiny, or Quarto, and configure them to display the results of their analysis. Kiosc runs the containers with the appropriate network configuration and acts as a proxy to the web services running inside the containers. We have been maintaining a Kiosc instance for more than 5 years, serving 321 containers in 150 projects across multiple institutions. In this article, we introduce the main functionality in Kiosc and describe four use-cases that show how Kiosc can prove helpful to the broader bioinformatics community, such as configuring and running web apps for the interactive visualization of workflow results, and publishing companion apps for scientific articles. Kiosc is a self-hosted platform for publishing web apps, which doesn't require significant expertise in either Docker or network administration to be deployed. It provides a similar service to Kubernetes, but with a convenient web interface and much lower administration overhead.

bioinformatics↗

Endothelial YAP/TAZ rewiring under cardiometabolic stress drives sex-divergent vascular remodeling in heart failure with preserved ejection fraction

Heart failure with preserved ejection fraction (HFpEF) is widely linked to endothelial dysfunction, yet the molecular pathways translating cardiometabolic stress into microvascular remodeling remain poorly defined. Here, we identify endothelial YAP/TAZ signaling as a mechanistic regulator of sex-divergent vascular responses in HFpEF. Plasma proteomics from the UK Biobank revealed elevated circulating YAP1 levels associated with heart failure and increased mortality, particularly in male patients, where YAP1 coincided with increased levels of the endothelial activation marker ESM1. In a hypertensive cardiorenal mouse model, endothelial YAP/TAZ deletion preserved cardiac function, whereas endothelial TAZ gain-of-function aggravated disease. Under cardiometabolic stress (TNF and high glucose), endothelial cells exhibited sex-specific rewiring of YAP/TAZ-dependent transcriptional programs. Male endothelial cells showed increased extracellular YAP1 release, angiogenic instability with impaired extracellular matrix remodeling, whereas female cells adopted an immune-primed, stress-adaptive phenotype. Mechanistically, cardiometabolic stress uncoupled canonical YAP-TEAD transcription and engaged alternative cofactors, including VGLL3 and VGLL4, thereby reshaping the endothelial secretome and propagating sex-divergent microvascular remodeling. These findings identify endothelial YAP/TAZ rewiring as a molecular switch that converts cardiometabolic stress into sex-divergent microvascular remodeling in HFpEF and connect this process to circulating YAP1 and ESM1 in patients.

cell biology↗

Diet and temperature interactively impact brown adipose tissue gene regulation controlled by DNA methylation

Controlling brown adipose tissue (BAT) plasticity in adulthood holds promising potential for effective new obesity therapies by targeting the mechanisms of adaptive thermogenesis. Recent studies have shown that BAT development and function are under epigenetic control, with DNA methylation linked to the regulation of key thermogenic and metabolic genes. Here we sought to understand how diet and cold exposure interactively shape BAT gene regulation controlled by DNA methylation. Mice (N = 8 per group) were housed under cold exposure (8{degrees}C) or thermoneutrality (30{degrees}C) and fed either chow or high-fat diet (HFD). BAT was isolated for transcriptome (RNAseq) and methylome (RRBS) analyses. We identified differentially methylated and expressed genes (DMEGs) by comparing the effects of cold exposure under chow and high-fat diet, as well as by analyzing the interaction between temperature and diet. Functional pathway enrichment and EpiFactors Database screening were used to assess epigenetic regulators, and candidate gene expression was validated by modulating DNA-methylation in vitro. We identified [~]1,360 differentially expressed genes (DEGs) uniquely affected by the diet-temperature interaction with most downregulated in HFD-fed mice, indicating that obesity limits the transcriptional response of BAT to cold. 65 DMEGs (4% of DEGs) were largely diet-specific in response to cold exposure, suggesting that DNA methylation contributes to a selective layer of gene regulation during BAT adaptation to distinct metabolic states. In HFD-fed mice, DMEGs were enriched in pathways related to mitochondrial dysfunction, altered lipid metabolism, neuroendocrine signaling, and compensatory stress responses, contrasting the adaptive thermogenic profile observed in chow-fed controls. Differentially expressed genes of epigenetic regulators such as Tet2, Dnmt3a and Apobec1 showed diet- and cold-dependent regulation, indicating impaired methylation flexibility under obesogenic conditions. Using cell culture experiments, we confirmed the regulation of gene expression of candidate genes, validating the functional link between DNA methylation and thermogenic gene regulation. This is the first study to demonstrate an epigenetic response to cold exposure that differs by dietary condition, particularly in obesity. Our findings highlight a coordinated transcriptional and epigenetic remodeling of BAT, shaped by both environmental and metabolic signals. These insights may inform targeted epigenetic or nutritional strategies to restore BAT function and would further strengthen our understanding of how these might be used as therapeutic basis to improve metabolic health in obesity. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=145 SRC="FIGDIR/small/672110v2_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@1f99b80org.highwire.dtl.DTLVardef@502d02org.highwire.dtl.DTLVardef@1bb0a93org.highwire.dtl.DTLVardef@b34e4c_HPS_FORMAT_FIGEXP M_FIG C_FIG Mice were housed under cold exposure or thermoneutrality and fed either chow or high-fat diet (HFD). RNA sequencing (RNAseq) and reduced representation bisulfite sequencing (RRBS) was performed on brown adipose tissue (BAT) which provide the fundament for the identification of differentially methylated positions (DMP) and regions (DMR) as well as differentially expressed genes (DEG) in three models: COLDchow, comparing 8{degrees} vs 30{degrees}C mice on chow diet; COLDHFD, comparing 8{degrees} vs 30{degrees}C mice on HFD diet and{Delta} COLDdiet, comparing COLDchow vs COLDHFD. Differentially methylated and expressed genes (DMEGs; circos plot shows a representative example) were identified for all comparisons based on those DMPs which correlated significantly with differentially expressed genes (DEGs; the heatmap shows a representative example). DMEGs were taken forward for pathways enrichment analyses and to identify differentially regulated epigenetic regulators using the EpiFactors Database. The figure was created with BioRender.

genomics↗

The Pseudomonas aeruginosa PrrF sRNAs promote biofilm formation at body temperature

Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen that causes both acute and chronic infections in vulnerable populations. Treatment of P. aeruginosa infections is increasingly challenging due to multi-drug resistance as well as biofilm formation that further increases antibiotic tolerance. Iron, which is sequestered by the host innate immune system, is also a key nutrient that required for P. aeruginosa biofilm formation. Previous work showed that the iron-responsive PrrF small regulatory RNAs (sRNAs), which are key to P. aeruginosas iron starvation response and required for virulence in murine lung infection, are dispensable for biofilm formation. However, these studies were performed using flow-cell biofilms at room temperature. Here we demonstrate a temperature dependency for PrrF in P. aeruginosa biofilm formation - the genes for these sRNAs are required for optimal biofilm formation at 37{degrees}C but not 25{degrees}C. We further show that the {Delta}prrF mutant lacks a yet-to-be identified surface appendage that is produced at 37{degrees}C but not 25{degrees}C. These studies demonstrate that the importance of the PrrF sRNAs in P. aeruginosa biofilm formation at body temperature and reveal a previously under-appreciated role of temperature in iron homeostasis and P. aeruginosa biofilm physiology. IMPORTANCEBiofilm formation is a critical aspect of pathogenesis for many microbial pathogens as it confers increased tolerance to the host immune system and antimicrobial treatments. Pseudomonas aeruginosa is an opportunistic pathogen that forms biofilms during infection, resulting in antimicrobial tolerance and treatment failure. Iron is a known requirement for P. aeruginosa biofilm formation, yet the precise role of iron homeostasis in biofilm physiology remains unclear. Here we show that temperature alters the requirement for the PrrF small regulatory RNAs, key components of P. aeruginosas iron starvation response, for biofilm formation. Specifically, PrrF is required for the optimal formation of biofilms in flow cells at 37{degrees}C but not 25{degrees}C, yet most flow-cell biofilm studies are conducted at 25{degrees}C. These results demonstrate a previously under-appreciated role of temperature in P. aeruginosa biofilm physiology.

microbiology↗

Osteopontin in colitis-associated carcinoma

Patients with ulcerative colitis (UC) and Crohns disease (CD) face a lifelong risk of developing colitis-associated carcinoma (CAC). Current insights into CAC development originate from murine CAC models, while human CAC studies primarily focus on mutational analysis of patient samples. Although the mutational landscape reveals distinct patterns and frequencies compared to colorectal cancer, it falls short in elucidating the inflammatory mechanisms of CAC development. Consequently, we adopted a multi-omics approach to unravel CAC carcinogenesis from an immunological perspective. Our data revealed a robust upregulation of SPP1 gene in CAC at both RNA and protein levels, expressed by CD68+ macrophages. In vitro OPN stimulation demonstrated no direct effect on intestinal epithelial organoids. However, the mutually exclusive spatial location of SPP1/OPN+ macrophages and CD8+ T cells suggests a crucial indirect role of SPP1/OPN in mediating an immunosuppressive tumour microenvironment.

cancer biology↗

Pharmacological inhibition of bromodomain and extra-terminal proteins induces NRF-2-mediated inhibition of SARS-CoV-2 replication and is subject to viral antagonism

Inhibitors of bromodomain and extra-terminal proteins (iBETs), including JQ-1, have been suggested as potential therapeutics against SARS-CoV-2 infection. However, molecular mechanisms underlying JQ-1-induced antiviral activity and its susceptibility to viral antagonism remain incompletely understood. iBET treatment transiently inhibited infection by SARS-CoV-2 variants and SARS-CoV, but not MERS-CoV. Our functional assays confirmed JQ-1-mediated downregulation of ACE2 expression and multi-omics analysis uncovered induction of an antiviral NRF-2-mediated cytoprotective response as an additional antiviral component of JQ-1 treatment. Serial passaging of SARS-CoV-2 in the presence of JQ-1 resulted in predominance of ORF6-deficient variants. JQ-1 antiviral activity was transient in human bronchial airway epithelial cells (hBAECs) treated prior to infection and absent when administered therapeutically. We propose that JQ-1 exerts pleiotropic effects that collectively induce a transient antiviral state that is ultimately nullified by an established SARS-CoV-2 infection, raising questions on their clinical suitability in the context of COVID-19.

microbiology↗

SODAR: enabling, modeling, and managing multi-omics integration studies

Scientists employing omics in life science studies face challenges such as the modeling of multi assay studies, recording of all relevant parameters, and managing many samples with their metadata. They must manage many large files that are the results of the assays or subsequent computation. Users with diverse backgrounds, ranging from computational scientists to wet-lab scientists, have dissimilar needs when it comes to data access, with programmatic interfaces being favored by the former and graphical ones by the latter. We introduce SODAR, the system for omics data access and retrieval. SODAR is a software package that addresses these challenges by providing a web-based graphical user interface for managing multi assay studies and describing them using the ISA (Investigation, Study, Assay) data model and the ISA-Tab file format. Data storage is handled using the iRODS data management system, which handles large quantities of files and substantial amounts of data. SODAR also offers programmable APIs and command line access for metadata and file storage. SODAR supports complex omics integration studies and can be easily installed. The software is written in Python 3 and freely available at https://github.com/bihealth/sodar-server under the MIT license.

bioinformatics↗

The need for alternative plant species interaction models

The limitations of classical Lotka-Volterra models for analyzing and interpreting competitive interactions among plant species have become increasingly clear in recent years. Three problems that have been identified are (1) the absence of frequency dependence, which is important for long-term coexistence of species, (2) the need to take unmeasured (often unmeasurable) variables influencing individual performance into account (e.g. spatial variation in soil nutrients or pathogens) and (3) the need to separate measurement error from biological variation. We modify the classical Lotka-Volterra competition models to address these limitations and we fit 8 alternative models to pin-point cover data on Festuca ovina and Agrostis capillaris over 3 years in a herbaceous plant community in Denmark, applying a Bayesian modelling framework to ascertain whether the model amendments improve the performance of the models and increase their ability to predict community dynamics and therefore to test hypotheses. Inclusion of frequency dependence and measurement error improved model performance greatly but taking possible unmeasured variables into account did not. Our results emphasize the importance of comparing alternative models in quantitative studies of plant community dynamics. Only by comparing alternative models can we identify the forces driving community assembly and change and improve our ability to predict the behavior of plant communities.

ecology↗

Effects of kin recognition on root traits of wheat germplasm over 100 years of breeding

Plant root and shoot growth has been shown to depend on the relatedness of co-cultivated genotypes, implying the existence of kin recognition mechanisms mediated by root exudates. If confirmed, this has important implications for crop breeding. We present the first large-sale investigation of kin recognition in a crop germplasm collection comprising 30 North-European cultivars and landraces of spring wheat, spanning 100 years of breeding history. In a full diallel in vitro bioassay, we compared root growth of seedlings when growing in pure substrate, or in substrate previously occupied by a donor seedling from the same (KIN) or another (NONKIN) genotype. Seedlings growing in KIN or NONKIN substrate generally had longer but not more roots than seedlings growing in pure substrate. Responses were generally larger in longer roots, suggesting that root elongation was promoted throughout the growth period. Responses to KIN and NONKIN substrates were found to range from positive to negative, with root length responses to kin being increasingly positive with year of release. Seedlings growing in KIN substrate generally had shorter but not fewer roots than seedlings growing in NONKIN substrate. This kin recognition ranged from positive to negative across the specific donor-receiver combinations and did not change systematically with year of release of either genotype. Root traits in both KIN and NONKIN substrate were affected by both donor and receiver genotype, and these effects were generally larger than the effect of specific combinations. Genotypes showing higher levels of kin recognition also tended to invoke larger responses in other genotypes. Kin recognition was reduced in most cases by the addition of sodiumorthovanadate, a chemical inhibitor, supporting the hypothesis that kin responses were mediated by changes in the chemical constitution of the substrate. The identified patterns of kin recognition across the germplasm collection were complex, suggesting a multigenic background and shared breeding history of the genotypes. We conclude that kin response represents a potential target for crop breeding which can improve root foraging and competitive interactions.

plant biology↗

Does metal pollution affect stoichiometry of soil-litter food webs?

To date the field of ecological stoichiometry has focused mainly on aquatic systems concentrating on macro-elements. We investigated terrestrial systems and included microelements to study the elemental transfer in the detritivorous food web. We compared food webs of six sites differing in the type and degree of metal pollution along two forest transects contaminated with copper or zinc. We measured 11 elements in litter, herbivores, detritivores, predators and omnivores. Based on elemental concentrations of elements differences between trophic groups were visualized using PCA. At all sites litter C:N, C:P, C:K and C:Na ratios were higher than in animals. Invertebrate trophic groups were significantly different from each other in C:Cu, C:Zn and C:Ca ratios. The calculated resource:consumer N:P ratio suggests that invertebrates in studied forests are N limited and not P limited. Similar patterns at all sites suggests that metal pollution at the studied intensity slightly affects the transfer of elements in the terrestrial macro-invertebrate food web.

ecology↗

Inhibition of host Lactate dehydrogenase A by a small-molecule limits Mycobacterium tuberculosis growth and potentiates bactericidal activity of isoniazid

Lactate dehydrogenase A (LDHA) mediates interconversion of pyruvate and lactate. Increased lactate turnover is shared by malignant and immune cells. Hypoxic lung granuloma in Mycobacterium tuberculosis-infected animals present elevated levels of Ldha and lactate. Such alteration in metabolic milieu could influence the outcome of interactions between M. tuberculosis and its infected immune cells. Given the central role of LDHA for tumorigenicity, targeting lactate metabolism is a promising approach for cancer therapy. Here, we sought to determine the importance of LDHA for Tuberculosis (TB) disease progression and its potential as a host-directed therapeutic target. To this end, we administered FX11, a small-molecule NADH-competitive LDHA inhibitor, to M. tuberculosis infected C57BL/6J mice and Nos2-/- mice with hypoxic necrotizing lung TB lesions mimicking human pathology more closely. FX11 did not inhibit M. tuberculosis growth in aerobic/hypoxic liquid culture, but modestly reduced the pulmonary bacterial burden in C57BL/6J mice. Intriguingly, FX11 administration limited M. tuberculosis replication and onset of necrotic lesions in Nos2-/- mice. In this model, Isoniazid (INH) monotherapy has been known to exhibit biphasic killing kinetics owing to the probable selection of an INH-tolerant subpopulation. This adverse effect was corrected by adjunct FX11 treatment and augmented the INH-derived bactericidal effect against M. tuberculosis. Our findings therefore support LDHA as a potential target for host-directed adjunctive TB therapy and encourage further investigations into the underlying mechanism.\n\nIMPORTANCETuberculosis (TB) continues to be a global health threat of critical dimension. Standard TB drug treatment is prolonged and cumbersome. Inappropriate treatment or non-compliance results in emergence of drug-resistant Mycobacterium tuberculosis strains (MDR-TB) that render current treatment options ineffective. Targeting the host immune system as adjunct therapy to augment bacterial clearance is attractive as it is also expected to be effective against MDR-TB. Here, we provide evidence that pharmaceutical blockade of host lactate dehydrogenase A (LDHA) by a small-molecule limits M. tuberculosis growth and reduces pathology. Notably, LDHA inhibition potentiates the effect of Isoniazid, a first-line anti-TB drug. Hence, its implications of our findings for short-term TB treatment are profound. In sum, our findings establish murine LDHA as a potential target for host-directed TB therapy.

microbiology↗

Analysis of immunological resistance to primary Mycobacterium tuberculosis infection in humans

BackgroundDespite recent advances in diagnosis and treatment, tuberculosis (TB) remains a major infectious disease killer in resource-poor settings. Strategies to prevent Mycobacterium tuberculosis (Mtb) infection are urgently required. By characterising natural protective immunity to Mtb infection we aimed to identify correlates of protection to guide vaccine development and other immune based therapies. MethodsTwo groups of Mtb-exposed contacts of TB patients were recruited in The Gambia and assessed for Mtb infection status using either tuberculin skin test (TST) reactivity at baseline and 3 months or QuantiFERON (QFT) reactivity at baseline and 6 months. For both groups, converters were defined as having a negative test at baseline and a positive one at follow-up, while those with a negative test at both time-points were defined as non-converters (Mtb resisters). Participants were analysed using RNA-sequencing and plasma Mtb proteome IgA and IgG arrays. ResultsSeveral genes were found to be differentially expressed at baseline between the groups prior to any signs of infection by current tests. Modular analysis revealed a distinct B cell gene signature in TST non-converters compared to converters (at q < 10-6, AUC > 0.7), which was only present in the most highly exposed group. Interestingly, when infection status was defined by QFT, enrichment of Type I IFN and antiviral gene signatures was observed. Plasma IgG and IgA antibody reactivity across the entire Mtb proteome showed the best differentiation in individuals with the highest exposure. An AUC of 1.0 (q<10-3) was observed for IgA reactivity to Rv0134 and an AUC of 0.98 for IgA reactivity to both Rv0629c and Rv2188c (all lower in TST non-converters). IgG reactivity to Rv3223c resulted in an AUC of 0.96 (q < 10-4) and was again lower in TST non-converters. The highest AUC for those with lower Mtb exposure were 0.84 (Rv2411c) for IgA and 0.83 (Rv2131c) for IgG. ConclusionsThese data provide insight into the early protective response to Mtb infection and possible avenues for novel therapeutic strategies to prevent Mtb infection.

immunology↗

The Aryl Hydrocarbon Receptor senses the Henna pigment Lawsone and mediates Yin-Yang effects on skin homeostasis

As a first host barrier, the skin is constantly exposed to environmental insults that perturb its integrity. Tight regulation of skin homeostasis is largely controlled by the aryl hydrocarbon receptor (AhR). Here, we demonstrate that Henna and its major pigment, the naphthoquinone Lawsone activate AhR, both in vitro and in vivo. In human keratinocytes and epidermis equivalents, Lawsone exposure enhances the production of late epidermal proteins, impacts keratinocyte differentiation and proliferation, and regulates skin inflammation. To determine the potential use of Lawsone for therapeutic application, we harnessed human, murine and zebrafish models. In skin regeneration models, Lawsone interferes with physiological tissue regeneration and inhibits wound healing. Conversely, in a human acute dermatitis model, topical application of a Lawsone-containing cream ameliorates skin irritation. Altogether, our study reveals how a widely used natural plant pigment is sensed by the host receptor AhR, and how the physiopathological context determines beneficial and detrimental outcomes.

cell biology↗