Publikationsfonds der Universität Hohenheim

Permanent URI for this collectionhttps://hohpublica.uni-hohenheim.de/handle/123456789/16624

Über den Publikationsfonds der Universität Hohenheim erhalten Wissenschaftlerinnen und Wissenschaftler der Universität finanzielle Unterstützung bei der Veröffentlichung ihrer Forschungsergebnisse im Open Access. Gefördert werden Zeitschriftenartikel in Fully-Open-Access-Zeitschriften (Gold-OA) und hybriden Subskriptionszeitschriften (Hybrid-OA) sowie Monografien. Autorinnen und Autoren können online einen Förderantrag zur Finanzierungsbeteiligung ihrer Publikation stellen.

Publikationsfonds: https://kim.uni-hohenheim.de/publikationsfonds
Förderantrag: https://kim.uni-hohenheim.de/foerderantrag

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Insect conservation in agricultural landscapes needs both high crop heterogeneity and semi-natural habitats
(2024) Tassoni, Sara; Becker, David; Kasten, Marit Kinga; Moriníere, Jérôme; Grass, Ingo
Identifying landscapes that are suitable for both biodiversity conservation and agricultural production is a major challenge. Traditionally, much research has focused on biodiversity conservation outside of agricultural production areas, e.g., in semi-natural habitats. In contrast, recent research has mainly focused on the potential of crop heterogeneity. This includes both compositional (crop diversity) and configurational heterogeneity (field border density). However, if and how crop heterogeneity, and semi-natural habitats interact to shape insect diversity in agricultural landscapes remains poorly understood. Here we investigated the combined effects of crop diversity, field border density, and semi-natural habitats (i.e., grassland proportion, hedge density) on insect diversity. We sampled insect communities from 14 – 17 June 2021 with pan traps in 27 study landscapes (500 m x 500 m) covering independent gradients of these landscape variables and identified a total of 587 insect species with DNA metabarcoding. We found that field border density mediated the effects of crop diversity, grassland proportion, and hedge density on insect richness. At low levels of field border density (i.e., landscapes with mostly large fields), effects were either neutral (crop diversity), negative (grassland proportion) or weakly positive (hedge density). By contrast, at high levels of field border density, crop diversity, grassland proportion, and hedge density all exerted positive effects on insect richness. Responses to crop heterogeneity and semi-natural habitat differed among trophic groups of insects (decomposers, herbivores, parasitoids, predators). While variation in richness of herbivorous insects followed the patterns of the overall richness, decomposer richness was not related to any of the investigated variables. Predator richness increased with hedge density in landscapes, whereas parasitoid richness increased when high levels of field border density and grassland proportion coincided. Our study shows that increasing crop heterogeneity is a viable strategy for promoting insect diversity in agricultural landscapes. However, the effects of the amount of remaining semi-natural habitats, such as grassland or hedges, are mediated by configurational heterogeneity, and vary between trophic groups. Efforts to conserve insects in agricultural landscapes must therefore focus on both increasing the heterogeneity of the crop matrix by promoting crop diversity and increasing the density of field borders, while also maintaining or restoring semi-natural habitats as important source habitats for insect species.
Metabolome fingerprinting reveals the presence of multiple nitrification inhibitors in biomass and root exudates of Thinopyrum intermedium
(2024) Issifu, Sulemana; Acharya, Prashamsha; Schöne, Jochen; Kaur-Bhambra, Jasmeet; Gubry-Rangin, Cecile; Rasche, Frank
Biological Nitrification Inhibition (BNI) encompasses primarily NH4 +-induced release of secondary metabolites to impede the rhizospheric nitrifying microbes from per- forming nitrification. The intermediate wheatgrass Thinopyrum intermedium (Kernza®) is known for exuding several nitrification inhibition traits, but its BNI potential has not yet been identified. We hypothesized Kernza® to evince BNI potential through the presence and release of multiple BNI metabolites. The presence of BNI metabolites in the biomass of Kernza® and annual winter wheat (Triticum aestivum) and in the root exudates of hydroponically grown Kernza®, were fingerprinted using HPLC-DAD and GC–MS/MS analyses. Growth bioassays involving ammonia-oxidizing bacteria (AOB) and archaea (AOA) strains were conducted to assess the influence of the crude root metabolome of Kernza® and selected metabolites on nitrification. In most instances, significant concentrations of various metabolites with BNI potential were observed in the leaf and root biomass of Kernza® compared to annual winter wheat. Furthermore, NH4 + nutrition triggered the exudation of various phenolic BNI metabolites. Crude root exudates of Kernza® inhibited multiple AOB strains and completely inhibited N. viennensis. Vanillic acid, caffeic acid, vanillin, and phenylalanine suppressed the growth of all AOB and AOA strains tested, and reduced soil nitrification, while syringic acid and 2,6-dihydroxybenzoic acid were ineffective. We demonstrated the considerable role of the Kernza® metabolome in suppressing nitrification through active exudation of multiple nitrification inhibitors.
Prostaglandin E2 signaling through prostaglandin E receptor subtype 2 and Nurr1 induces fibroblast growth factor 23 production
(2024) Feger, Martina; Hammerschmidt, Katharina; Liesche, lona; Rausch, Steffen; Alber, Jana; Föller, Michael
Bone cells produce fibroblast growth factor 23 (FGF23), a hormone regulating renal phosphate and vitamin D homeostasis, and a paracrine factor produced in further tissues. Chronic kidney disease and cardiovascular disorders are associated with early elevations of plasma FGF23 levels associated with clinical outcomes. FGF23 production is dependent on many conditions including inflammation. Prostaglandin E2 (PGE2) is a major eicosanoid with a broad role in pain, inflammation, and fever. Moreover, it regulates renal blood flow, renin secretion, natriuresis as well as bone formation through prostaglandin E receptor 2 (EP2). Here, we studied the role of PGE2 and its signaling for the production of FGF23. Osteoblast-like UMR-106 cells were exposed to EP receptor agonists, antagonists or RNAi. Wild type and EP2 knockout mice were treated with stable EP2 agonist misoprostol. Fgf23 or Nurr1 gene expression was determined by quantitative real-time PCR, hormone and further blood parameters by enzyme-linked immunosorbent assay and colorimetric methods. PGE2 and EP2 agonists misoprostol and butaprost enhanced FGF23 production in UMR-106 cells, effects mediated by EP2 and transcription factor Nurr1. A single dose of misoprostol up-regulated bone Fgf23 expression and FGF23 serum levels in wild type mice with subtle effects on parameters of mineral metabolism only. Compared to wild type mice, the FGF23 effect of misoprostol was significantly lower in EP2-deficient mice. To conclude, PGE2 signaling through EP2 and Nurr1 induces FGF23 production. Given the broad physiological and pathophysiological implications of PGE2 signaling, this effect is likely of clinical relevance.
tsCRISPR based identification of Rab proteins required for the recycling of Drosophila TRPL ion channel
(2024) Zeger, Matthias; Stanisławczyk, Lena Sarah; Bulić,Marija; Binder, Andrea Maria; Huber, Armin
In polarized cells, the precise regulation of protein transport to and from the plasma membrane is crucial to maintain cellular function. Dysregulation of intracellular protein transport in neurons can lead to neurodegenerative diseases such as Retinitis Pigmentosa, Alzheimer’s and Parkinson’s disease. Here we used the light-dependent transport of the TRPL (transient receptor potential-like) ion channel in Drosophila photoreceptor cells to study the role of Rab proteins in TRPL recycling. TRPL is located in the rhabdomeric membrane of dark-adapted flies, but it is transported out of the rhabdomere upon light exposure and localizes at the Endoplasmatic Reticulum within 12 h. Upon subsequent dark adaptation, TRPL is recycled back to the rhabdomeric membrane within 90 min. To screen for Rab proteins involved in TRPL recycling, we established a tissue specific (ts) CRISPR/Cas9-mediated knock- out of individual Rab genes in Drosophila photoreceptors and assessed TRPL localization using an eGFP tagged TRPL protein in the intact eyes of these mutants. We observed severe TRPL recycling defects in the knockouts of Rab3, Rab4, Rab7, Rab32, and RabX2. Using immunohistochemistry, we further showed that Rab3 and RabX2 each play a significant role in TRPL recycling and also influence TRPL transport. We localized Rab3 to the late endosome in Drosophila photoreceptors and observed disruption of TRPL transport to the ER in Rab3 knock-out mutants. TRPL transport from the ER to the rhabdomere ensues from the trans-Golgi where RabX2 is located. We observed accumulated TRPL at the trans-Golgi in RabX2 knock-out mutants. In summary, our study reveals the requirement of specific Rab proteins for different steps of TRPL transport in photoreceptor cells and provides evidence for a unique retrograde recycling pathway of TRPL from the ER via the trans-Golgi

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