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Trautmann, S.

Publications and source records attributed to Trautmann, S..

4 recordsLinked to original sources

Spatial overlap and phenotypic similarity predict hybridisation in birds

Hybridisation is widespread in birds and has important eco-evolutionary implications. Historically, much research has focused on the consequences of hybridisation. To date, however, far less attention has been paid to the causes of hybridisation and, in particular, why particular pairs of species form hybrids. Using large-scale comparative analyses, we find that similarity in plumage, vocalisations, and morphometric traits, as well as evolutionary relatedness, drive hybridisation in North American and European birds. In passerines, the avian order including songbirds, similarity in vocalisations and morphology are the key phenotypic predictors of hybridisation, whereas in non-passerines, species pairs with similar plumage and morphology are more likely to hybridise. We also find that the likelihood of hybrid formation increases with the magnitude of range and habitat overlap, demonstrating that hybridisation is not just a product of occasional contact between closely related species. Our findings have important conservation implications in this age of rapid anthropogenic change and species reassembly.

evolutionary biology↗

Analysing bird population trends from monitoring data with highly structured sampling designs

Population trends derived from systematic monitoring programmes are essential to identify species of conservation concern and to evaluate conservation measures. However, monitoring data pose several challenges for statistical analysis, including spatial bias due to an unbalanced sampling of natural regions or habitats, variation in observer expertise, frequent observer changes, and overdispersion or zero-inflation in the raw data. An additional challenge arises from so-called rolling survey designs, where each site is only visited once within each multi-year rotation cycle. We developed a GAMM-based workflow that addresses these challenges and exemplify its application with the highly structured data from the Ecological Area Sampling (EAS) in the German federal state North Rhine-Westphalia (NRW). First, we derive a routine that allows informed decisions about the most appropriate combination of distribution family (Poisson or negative binomial), model covariates (e.g., habitat characteristics), and zero-inflation formulations to reflect species-specific data distributions. Second, we develop a correction factor that buffers population trend estimates for variation in observer expertise as reflected in variation in total bird abundance. Third, we integrate region-specific trends that adjust for between-year variation in the representation of habitat or natural regions within the yearly subset of sampled sites. In a consistency check, we found good match between our GAMM-based EAS trends and TRIM-based trends from the German Common Bird Monitoring scheme. The study provides a template script for R statistical software so the workflow can be adapted to other monitoring programmes with comparable survey designs and data structures.

ecology↗

Abnormal molecular signatures of inflammation, energy metabolism and vesicle biology in human Huntington disease peripheral tissues

BackgroundA major challenge in neurodegenerative diseases concerns identifying biological disease signatures that track with disease progression or respond to an intervention. Several clinical trials in Huntington disease (HD), an inherited, progressive neurodegenerative disease, are currently ongoing. Therefore, we examined whether peripheral tissues can serve as a source of readily accessible biological signatures at the RNA and protein level in HD patients. ResultsWe generated large, high-quality human datasets from skeletal muscle, skin and adipose tissue to probe molecular changes in human premanifest and early manifest HD patients - those most likely involved in clinical trials. In-depth single nucleotide polymorphism data across the HTT gene will facilitate the use of the generated primary- and iPSC cell lines in allele-specific targeting approaches. The analysis of the transcriptomics and proteomics data shows robust, stage-dependent dysregulation. Gene ontology analysis confirmed the involvement of inflammation and energy metabolism in peripheral HD pathogenesis. Furthermore, we observed changes in the homeostasis of extracellular vesicles, where we found consistent changes of genes and proteins involved in this process. ConclusionsOur omics data document the involvement of inflammation, energy metabolism and extracellular vesicle homeostasis. This demonstrates the potential to identify biological signatures from peripheral tissues in HD suitable as biomarkers in clinical trials. Together with the primary cell lines established from peripheral tissues and a large panel of iPSC lines that can serve as human models of HD, the generated data are a valuable and unique resource to advance the current understanding of molecular mechanisms driving HD pathogenesis.

neuroscience↗

Autophagy activation, lipotoxicity and lysosomal membrane permeabilization synergize to promote pimozide- and loperamide-induced glioma cell death

Increasing evidence suggests that induction of lethal autophagy carries potential significance for the treatment of glioblastoma (GBM). In continuation of previous work, we demonstrate that pimozide and loperamide trigger an ATG5- and ATG7-dependent type of cell death that is significantly inhibited with the cathepsin inhibitors E64D/Pepstatin A and the lipid ROS scavenger -tocopherol in MZ-54 GBM cells. Global proteomic analysis after treatment with both drugs also revealed an increase of proteins related to lipid and cholesterol metabolic processes. These changes were accompanied by AKT1 (AKT serine/threonine kinase 1) inhibition and a massive accumulation of cholesterol and other lipids in the lysosomal compartment, indicative of impaired lipid transport/degradation. In line with these observations, pimozide and loperamide treatment were associated with a pronounced increase of bioactive sphingolipids including ceramides, glucosylceramides and sphingoid bases measured by targeted lipidomic analysis. Furthermore, pimozide and loperamide inhibited the activity of acid sphingomyelinase (ASM), increased lipid-ROS levels and promoted induction of lysosomal membrane permeabilization (LMP), as well as release of cathepsin B into the cytosol in MZ-54 wt cells. While LMP and cell death were significantly attenuated in ATG5/7 KO cells, both events were enhanced by depletion of the lysophagy receptor VCP (valosin containing protein), supporting a pro-survival function of lysophagy under these conditions. Collectively, our data suggest that pimozide and loperamide-driven autophagy and lipotoxicity synergize to induce LMP and lysosomal cell death. The results also support the notion that simultaneous overactivation of autophagy and induction of LMP represents a promising approach for the treatment of GBM.

cancer biology↗