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Bergman, O.

Publications and source records attributed to Bergman, O..

5 recordsLinked to original sources

Skin lipid chemistry influences host-microbiome-pathogen interactions in snake fungal disease (ophidiomycosis)

Within host-microbiome-pathogen systems, the host chemical microenvironment is often overlooked despite its inherent role in host physiology. We used a multifaceted experimental approach encompassing culture-dependent and independent methods, metagenomic and genomic data, and deep neural network modeling to assess the impact of host skin lipid chemistry and the bacterial microbiome on the growth of Ophidiomyces ophidiicola (ophidiomycosis, snake fungal disease). Results suggest that host skin lipid chemistry (e.g., oleic acid, squalene) and bacteria isolated from wild snake skins (e.g., Chryseobacterium sp. and Stenotrophomonas maltophilia) suppress O. ophidiicola growth. Notably, the O. ophidiicola genome contains biosynthetic gene clusters (BGCs) that encode metabolites that may suppress host lipid production, facilitating fungal pathogenicity. The contrastive deep neural network produced a near-perfect alignment of snake skin lipid and microbiome profiles for both individual snakes and disease states. BGCs from bacterial genomes isolated from snake skin overlap with metagenome profiles from wild snakes and correlate with disease state. We highlight antifungal activity found in the diverse lipid milieu of snake skin and bacterial-fungal interactions (BFIs) that structure the skin microbiome. Our results illustrate a strong relationship among a fungal pathogen, the microbiome, and host skin lipid chemistry.

microbiology↗

Complex nitrogen redox couplings control methane emissions from Arctic upland yedoma taliks

Yedoma-permafrost holds disproportionately large carbon and nitrogen pools, concentrated in icy, Pleistocene-aged silt deposits in the Arctic. Upon thaw, these undergo microbial mineralization, releasing greenhouse gases (GHGs) including carbon-dioxide (CO2), methane (CH4) and nitrous-oxide (N2O). Here we present combined geochemical data with microbial function and community dynamics from deep-talik soil boreholes in an unsaturated yedoma upland. Our results reveal significant in-situ spatio-temporal seasonal shifts in microbial functional, community composition and diversity within 7-m deep upland talik. In situ methanogenesis persisted in the soil talik throughout the year due to the permafrost thaw. In the winter methanotrophy was negligible within and above the methanogenic zone, leading to elevated CH4 emissions to the atmosphere. This is likely due to reduced microbial methanotrophic activity, associated with lower temperatures and nitrogen availability. During summer, at and above the anoxic methanogenic zone, nitrate/nitrite mediated anaerobic oxidation of methane (N-AOM) by ANME2d and the NC-10 phylum, together with aerobic methanotrophy near the soil surface, significantly attenuated CH4 emissions. Nitrous-oxide concentrations peaked at 10 cm (7.2 {micro}M) and 105 cm (6.7 {micro}M) and were associated with denitrification and N-AOM by Methanoperedens (ANME2d). In the summer only and within the top 1 m of soil, high expression of nitrogen related genes (narG, norB, amoA, Annamox, and Feammox) indicated active redox dynamics, potentially providing nitrogen species for N-AOM. The potential N2O emissions in summer may imply higher net GHGs emission from yedoma uplands as climate warming leads to longer summers and warmer soils in the future.

microbiology↗

Unveiling the Ecology of Legionella in a Stratified Freshwater Lake: Seasonal Dynamics, Host Interactions, and Persistence Under Oxygen Limited Conditions

AbstractO_ST_ABSBackgroundC_ST_ABSLegionella are predominantly recognized as aerobic pathogens in man-made water systems. However, their potential persistence in natural freshwater environments, particularly under oxygen limited conditions, remains poorly explored. In this study we investigated the spatio-temporal dynamics of Legionella occurrence in a seasonally stratified sub-tropical freshwater lake, with a focus on anaerobic conditions of the anoxic hypolimnion. ResultsOur study reveals significant seasonal variations in Legionella absolute abundance, with the highest concentrations occurring during and immediately following lake mixing events. Unexpectedly, high levels of Legionella were measured in the anaerobic hypolimnion layer of the lake. Utilizing genus specific amplicon-based sequencing, we found significant shifts in Legionella community composition, that are related to the sampling month. Several environmental factors were associated with the observed changes, including temperature, DO, chlorophyll and dinoflagellate biomass. Moreover, we identified Legionella genotypes unique to samples presenting hypoxic conditions - that were not closely related to known Legionella species. In addition, we noted genotypes present in anoxic samples, that were absent from the oxic layers of the corresponding sampling dates. These results were accompanied by changes in the interaction patterns between Legionella and their potential hosts, in oxic and anoxic conditions. ConclusionsThis study challenges the conventional view of Legionella as a strictly aerobic pathogen by demonstrating its persistence in anoxic freshwater environments. Our findings suggest that certain Legionella species may have adapted to low- oxygen conditions, potentially through alternate metabolic pathways or by residing within protozoan hosts. The identification of unique Legionella genotypes in the hypolimnion, along with shifts in occurrence, diversity, and host interactions, underscores the complexity of Legionella ecology. These results highlight the need for further research on Legionella in natural freshwater systems, which serve as reservoirs for the bacteria and potential sources for human infection. Further investigation into the mechanisms underlying Legionella persistence in anaerobic conditions and its interactions with environmental hosts is essential for a better understanding of the evolutionary forces shaping this family of human pathogens.

ecology↗

The junctional mechanosensor AmotL2 regulates YAP promotor accessibility

Endothelial cells (ECs) are constantly exposed to mechanical forces in the form of fluid shear stress, extracellular stiffness, and cyclic strain. How these forces are sensed by ECs remains an understudied aspect in the homeostatic regulation of the circulatory system. Angiomotin-like 2 (AmotL2) is localised to EC junctions and is required for alignment and actin reorganisation under conditions of high shear stress. Here we show that AmotL2 crucially regulates transcription and promotor activity of the YAP gene. Functionally, density-dependent proliferation of ECs in vitro and proliferation of a subpopulation of ECs within the inner aortic arch, were both reliant on AmotL2 and Yap/Taz endothelial expression in vivo. Mechanistically, depletion of AmotL2 led to altered nuclear morphology, chromatin accessibility and suppression of YAP-promotor activity through increased H3K27me3 mediated by the polycromb repressive complex component EZH2. Our data describe a previously unknown role for junctional mechanotransduction in shaping the epigenetic landscape and transcriptional regulation of YAP in vascular homeostasis.

cell biology↗

The VE-cadherin/AmotL2 mechanosensory pathway suppresses aortic inflammation and the formation of abdominal aortic aneurysms

Arterial endothelial cells (ECs) have the ability to respond to mechanical forces exerted by fluid shear stress. This response is of importance, as it is protective against vascular diseases such as atherosclerosis and aortic aneurysms. Mechanical forces are transmitted at the sites of adhesion to the basal membrane as well as cell-cell junctions where protein complexes connect to the cellular cytoskeleton to relay force into the cell. Here we present a novel protein complex that connects junctional VE-cadherin and radial actin filaments to the LINC complex in the nuclear membrane. We show that the scaffold protein AmotL2 is essential for the formation of radial actin filaments and the flow-induced alignment of aortic and arterial ECs. The deletion of endothelial AmotL2 alters nuclear shape as well as subcellular positioning. Molecular analysis shows that VE-cadherin is mechanically associated with the nuclear membrane via binding to AmotL2 and Actin. Furthermore, the deletion of AmotL2 in ECs provokes a pro-inflammatory response and abdominal aortic aneurysms (AAA) in the aorta of mice on a normal diet. Remarkably, transcriptome analysis of AAA samples from human patients revealed a negative correlation between AmotL2 expression and aneurysm diameters, as well as a positive correlation between AmotL2 and YAP expression. These findings provide a conceptual framework regarding how mechanotransduction in the junctions is coupled with vascular disease.

cell biology↗