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Buder, K.

Publications and source records attributed to Buder, K..

4 recordsLinked to original sources

Virus-host interactions on volcanic ash from Mount Etna

Volcanic ash represents an extreme and dynamic habitat, yet it hosts diverse microbial communities with largely unexplored viral diversity. This study investigated bacterial and viral populations in volcanic ash from Mount Etna (Italy) collected during the eruption, focusing on microbial novelty, activity, and virus-host interactions. Taxonomic profiling revealed that Pseudomonas and Telluria were the dominant bacterial genera, both frequently detected in airborne environments. In contrast, enrichment cultures with volcanic ash were dominated by spore-forming members of the phylum Bacillota, highlighting their resilience under harsh conditions. Metagenomic analysis recovered 19 high-quality metagenome-assembled genomes, including four previously undescribed bacterial species. Replication rate estimates showed that certain taxa were metabolically active, particularly at one sampling site. The presence of Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) systems with spacers matching viral sequences suggested viral predation pressure on volcanic ash. A total of 1139 viral operational taxonomic units (vOTUs) were identified, of only around half (660 vOTUs) showed similarities to known phages, underscoring the presence of novel viruses. Shared vOTUs across sites revealed the presence of both a core virome and site-specific viral populations. Virus-host predictions indicated frequent interactions with hosts from multiple Gammaproteobacterial genera. Additionally, a 336 kb jumbo phage genome exhibited extensive metabolic capabilities and genetic autonomy. Experimental work identified a unique lytic Bacillus-infecting phage ("Phoenix") with limited propagation capacity. Furthermore, prophage induction experiments revealed active, morphologically diverse temperate phages across multiple bacterial host strains. Overall, these findings highlight volcanic ash as a reservoir of microbial and viral diversity, shaped by environmental extremes and dynamic ecological interactions. HighlightsMetagenomic and cultivation experiments were used to study viruses on volcanic ash Novelty of viral and bacterial species was detected Viral-bacterial interactions in metagenomes from volcanic ash were detected Cultivatable bacteria were mainly spore-forming Bacilli species and harbored inducible prophages

microbiology↗

Virus-host interactions and viral population dynamics across atmospheric cloud events

BackgroundCloud water harbors diverse microbial communities despite its extreme oligotrophic conditions. However, the ecological and evolutionary dynamics of viruses in these transient atmospheric habitats remain poorly understood. Clouds have traditionally been regarded primarily as passive carriers of microorganisms rather than as active ecological environments supporting microbial interactions. In this study, cloud water was sampled at Mount Verde, Cape Verde Islands (744 m a.s.l.). We performed metagenomic analyses of iron-flocculated cloud water alongside genome analyses of a bacterial isolate and metagenome-assembled genomes using established bioinformatic approaches. Viral diversity, virus-host interactions, metabolic functions, genetic adaptations, and viral population dynamics across cloud events were investigated. In addition, UV-B resistance experiments were conducted for a novel cloud-water isolate. ResultsWe isolated 24 cloud water bacteria, including four novel species lineages, and recovered 62 high-quality metagenome-assembled genomes, including 10 novel species lineages. We identified 458 viral operational taxonomic units and 237 virus-host linkages across diverse prokaryotic hosts, revealing active viral predation across diverse bacterial taxa. In addition, CRISPR spacer matches from isolates of novel bacterial lineages such as Deinococcus nubigenus MPC36 were found. Viruses carried genes involved in host adaptation to environmental stressors, including cold-shock response, UV radiation resistance, and osmotic stress. In addition, viral populations exhibited SNP-level microdiversity and shifts in single-nucleotide variant composition across temporally proximate cloud events, indicating rapid population turnover. Experimental characterization of the cloud isolate Curtobacterium nubigenum MPC39 further revealed pronounced resistance to UV-B radiation and the presence of an inducible prophage, Curtobacterium phage vB_CnuS_Cirrus1 assigned to the new viral family Nebulaviridae, which could be validated in transmission electron microscopy. Reconstructed genomes from cloud-associated bacteria encoded carbon monoxide dehydrogenase genes and UV resistance genes, suggesting trace gas metabolism and enhanced UV protection as survival strategies in oligotrophic cloud droplets. In silico replication rates estimated using iRep were consistent with active bacterial replication at the time of sampling. ConclusionsTogether, these findings demonstrate that clouds are not merely passive carriers of microorganisms, but dynamic atmospheric ecosystems in which virus-host interactions shape microbial diversity and contribute to microbial turnover, atmospheric dispersal, and cloud-water biogeochemistry.

microbiology↗

Structural Basis for OAS2 Regulation and its Antiviral Function

Oligoadenylate synthetase (OAS) proteins are immune sensors for double-stranded RNA and critical for restricting viruses. OAS2 comprises two OAS domains, only one of which can synthesize 2-5-oligoadenylates for RNase L activation. Existing structures of OAS1 provide a model for enzyme activation, but do not explain how multiple OAS domains discriminate RNA length. Here, we discover that OAS2 exists in an autoinhibited state as a zinc-mediated dimer and present a mechanism for RNA length discrimination: the catalytically deficient domain acts as a molecular ruler that prevents autoreactivity to short RNAs. We demonstrate that dimerization and myristoylation localize OAS2 to Golgi membranes and that this is required for OAS2 activation and restriction of viruses that exploit the endomembrane system for replication, e.g. coronaviruses. Finally, our results highlight the non-redundant role of OAS proteins and emphasize the clinical relevance of OAS2 by identifying a patient with a loss-of-function mutation leading to autoimmune disease.

biochemistry↗

Disrupted Sphingosine-1-Phosphate Homeostasis Drives Nephrotoxicity in Sphingosine-1-Phosphate Lyase Insufficiency Syndrome (SPLIS)

Sphingosine-1-phosphate lyase insufficiency syndrome (SPLIS), also known as nephrotic syndrome type 14 (NPHS14), is an autosomal recessive disorder characterized by renal, neurological, dermatological, endocrine, and immunological symptoms. This condition is caused by loss-of-function mutations in the SGPL1 gene, which encodes sphingosine-1-phosphate lyase (SGPL1p/SPL), the enzyme responsible for the terminal degradation of sphingosine-1-phosphate (S1P) in sphingolipid catabolism. We investigated a novel case of SPLIS associated with a recently reported SGPL1 mutation (c.1084T>A; p.Ser362Thr). Using stable isotope flux analyses, we demonstrated in patient-derived fibroblasts and HEK293T SGPL1 knockout models that SGPL1p deficiency does not consistently result in pathological S1P accumulation. Instead, SPL-deficient cells are able to maintain steady-state S1P levels through two compensatory mechanisms: O_LIRegulation of de novo sphingolipid synthesis via the ORMDL-ceramide axis. C_LIO_LIIncreased conversion of excess ceramides into glycosphingolipids. C_LI However, when steady-state conditions are disrupted--either by external sphingolipid supplementation or by impairing homeostatic control--a pathological increase in intracellular S1P occurs in SPL-deficient cells. In vivo, Sgpl1-/-mice exhibited significant urinary excretion of S1P and marked S1P enrichment in the kidneys. This pathological accumulation of S1P dysregulates cytoskeletal homeostasis, impairing renal epithelial formation. Based on these findings, we hypothesize that the reabsorption of urinary S1P contributes to toxic renal accumulation, providing an explanation for the nephrotoxicity observed in SPLIS and its association with nephrotic syndrome. Importantly, we found that the cytoskeletal disruptions could be mitigated by inhibiting the Rho-ROCK signaling pathway using the clinically approved inhibitor Fasudil. These findings illuminate the pathophysiological basis of SPLIS nephrotoxicity and propose a promising pharmacological intervention strategy. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=144 SRC="FIGDIR/small/634100v1_ufig1.gif" ALT="Figure 1"> View larger version (24K): org.highwire.dtl.DTLVardef@e70e68org.highwire.dtl.DTLVardef@1630198org.highwire.dtl.DTLVardef@fde277org.highwire.dtl.DTLVardef@1f2b8e_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗