Biology subjects

Schenk, H.

Publications and source records attributed to Schenk, H..

9 recordsLinked to original sources

bioRxiv2026

Development and parameterisation of a size-structured multispecies bioeconomic model integrating consumer demand

A high proportion of the world's population relies on marine fisheries as a source of food and employment, highlighting the need for sustainable exploitation strategies. However, fisheries management commonly relies on single-species models that overlook ecological interactions and economic trade-offs, which may lead to stocks being exploited above sustainable levels. To address this gap, we developed a novel size-structured, multispecies bioeconomic module integrated within the spatially explicit, individual-based OSMOSE ecosystem model. OSMOSE represents exploited fish communities in which individuals interact through opportunistic, size-dependent predator-prey interactions which are explicitly incorporated into the bioeconomic framework. The bioeconomic model accounts for multiple species and size classes, allowing for size-dependent market prices. Fishing costs and profits are represented using an extension of the Gordon-Schaefer model to multiple interacting species, while consumer demand is modelled using a nested Dixit-Stiglitz utility function with three levels of constant elasticity of substitution for fish commodity, species and size classes. We present a method for estimating parameters for the bioeconomic module when empirical estimates are unavailable, using the North Sea OSMOSE configuration, which comprises 15 species. Our method successfully estimated the six bioeconomic parameters required to operationalise the model. Results indicate that differences in cost parameters were primarily associated with variability in species biomass rather than fishing gear, while fish prices were more strongly influenced by consumer's demand than by availability. This framework provides a basis for assessing the economic consequences of alternative climate change scenarios and supporting sustainable fisheries management.

ecology↗

bioRxiv2026

Injury-induced Cxcl11 and neutrophil signaling drive zebrafish kidney regeneration by generating a nephrogenic niche of Fgf and Wnt expression

Adult zebrafish regenerate their kidneys after injury by activating quiescent renal stem cells, however the injury signals that activate kidney stem cells are not known. We show here that an innate immune, cytokine response after tubule injury is required and sufficient to induce adult zebrafish kidney regeneration. An injury reporter zebrafish transgenic, Tg(kim1:mScarlet3), revealed that tubule injury occurred specifically in kidney proximal tubules and was associated with a rapid accumulation of neutrophils and macrophages. Injury also activated a Tg(NFkB:GFP) reporter transgene specifically in kidney tubules where RNA seq revealed NFkB target gene and cytokine expression. Inhibition of NFkB signaling with JSH-23 blocked Tg(NFkB:GFP) reporter activation and also inhibited induction of new nephrons. Systemic injection of the immune activators lipopolysaccharide or zymosan into uninjured fish rapidly induced cytokine expression followed by nephrogenic gene expression and the appearance of new, functional nephrons. Analysis of injury-induced cytokines revealed that several paralogs of cxcl11 were strongly expressed throughout the regeneration response and injection of recombinant Cxcl11 was sufficient to induce FGF-dependent kidney stem cell aggregation, but not Wnt-dependent epithelial differentiation. Kidney injury in zebrafish expressing a neutrophil dominant negative rac2D57N transgene activated Fgf signaling but failed to induce wnt9b or downstream Wnt target genes. Nephrogenic gene expression and epithelial tubule formation was rescued by treatment with the canonical Wnt agonist CHIR. Our findings demonstrate that an injury-induced, sterile immune response regulates kidney regeneration by establishing a nephrogenic niche of Fgf and Wnt signaling that supports tissue-resident kidney stem cell differentiation into functional nephrons.

developmental biology↗

bioRxiv2025

Large-scale wearable data reveal spatiotemporal organization of annual sleep patterns

Sleep is fundamental to health, yet large-scale, objective data on how geography shapes sleep behavior remain scarce. We analyzed over 45 million nights of sensor data from 105,741 German adults wearing consumer-grade wearables across 2.7 years. Sleep timing displayed a continuous east-west gradient, with later onset, midsleep, and offset in western regions, consistent with solar progression. This effect was strongest on weekends and in rural areas, where midsleep was delayed by 2.2 minutes per degree longitude and sleep duration increased by 1.0 minute. A north-south gradient also emerged. Weekday midsleep advanced by 0.9 minutes per degree latitude, while weekend midsleep was delayed by 0.2 minutes, resulting in greater social jetlag in the north. Sleep duration declined toward higher latitudes across both day types. Seasonal analyses revealed consistent annual rhythms. Sleep duration increased by 24.7 minutes in winter relative to summer, and sleep offset closely followed sunrise. These patterns highlight the joint influence of solar and social time on sleep, with implications for regionally tailored public health strategies.

neuroscience↗

bioRxiv2025

Multiple Wnt signaling pathways direct epithelial tubule interconnection in the regenerating zebrafish kidney

Epithelial tubule fusion is fundamental for kidney morphogenesis. Differentiating nephron tubules interconnect with collecting system epithelia to generate a lumenal pathway for fluid excretion. In the adult zebrafish kidney, nephrogenesis occurs as a regenerative response to injury and provides a model to explore cell signaling pathways required for tubule interconnection. We show that canonical Wnt signaling at the junction between two tubules induces a mesenchymal, invasive cell phenotype and is required, along with Src kinase and rac1, to generate basal cell protrusions. The Wnt ligands wnt9b and wnt4 are both required for new nephron formation after injury. Mutation in wnt4 or treatment with the canonical Wnt inhibitor IWR1 blocks formation of basal protrusions in forming nephrons. Mutation in the Wnt receptor frizzled9b reveals a fusion-associated non-canonical Wnt pathway that acts to 1) restrict canonical Wnt gene expression, 2) drive Rho kinase-dependent apical constriction of epithelial cells, and 3) position basal protrusions and generate orthogonal tubule lumenal connections. As a result, frizzled9b mutant nephrons fail to fully interconnect with target distal tubules. Our results indicate that canonical and non-canonical Wnt signaling interact in the same cells to orient and drive tubule interconnection in the regenerating zebrafish kidney.

developmental biology↗

bioRxiv2024

Multi-objective management of naturally regenerating beech forests: An ecological-economic optimization approach

How can we meet economic objectives of timber harvesting while maintaining the functioning of diverse forest ecosystems? Existing forest models that address this type of question are often complex, data-intensive, challenging to couple with economic optimization models, or can not easily be generalised for uneven-aged mixed-species forests. Here, we develop an ecological-economic optimization model, which integrates a state-of-the-art demographic forest model with a continuous cover forestry harvesting model to optimise efficient and sustainable timber harvesting. As a proof-of-concept, we apply the model to a beech-dominated forest in the Hainich-Dun region in Thuringia, Germany, with the goal of optimising multiple objectives such as timber yield and the biodiversity value of the forest. The ecological module is the Perfect Plasticity Approximation (PPA) demographic forest model that simulates forest dynamics based on individual tree growth and survival rates in the canopy and understory layers, respectively, as well as recruitment rates. We used repeated forest inventory data from a 28-ha forest plot to quantify these demographic rates and validated the predictions of the ecological module against the structure of old-growth beech forests in Europe. The economic module includes the optimization of net revenues (market revenues net of harvesting cost) from harvesting timber. As an indicator of the biodiversity value of the forest, we use the number of retained habitat trees (>70 cm diameter). The forest model delivered reasonable predictions of structural attributes of unmanaged old-growth beech forests. When net revenues from timber harvest were maximised, trees were logged when they reached 55 cm in diameter. This is similar to current management practices in beech forests. We found a linear trade-off between timber net revenues and biodiversity value with about 2.5% of the maximum benefit of timber harvest being lost with each additionally retained habitat tree. We established a generic ecological-economic modelling framework that reliably represents forest dynamics as well as optimising forest management. To our knowledge, this is the first forest model for central European forests capable of identifying optimal harvesting over the full set of feasible strategies, rather than merely comparing predefined management scenarios. The framework can be extended to mixed-species forests and support forest management for diverse ecosystem services.

ecology↗

bioRxiv2019

Calcium dobesilate reduces VEGF signaling by interfering with heparan sulfate binding site and protects from vascular complications in diabetic mice

Inhibiting vascular endothelial growth factor (VEGF) is a therapeutic option in diabetic microangiopathy. However, VEGF is needed at physiological concentrations to maintain glomerular integrity; complete VEGF blockade has deleterious effects on glomerular structure and function. Anti-VEGF therapy in diabetes raises the challenge of reducing VEGF-induced pathology without accelerating endothelial cell injury. Heparan sulfate (HS) can act as a co-receptor for VEGF. Calcium dobesilate (CaD) is a small molecule with vasoprotective properties that has been used for the treatment of diabetic microangiopathy. Preliminary evidence suggests that CaD interferes with HS binding sites of fibroblast growth factor. We therefore tested the hypotheses that (1) CaD inhibits VEGF signaling in endothelial cells, (2) that this effect is mediated via interference between CaD and HS, and (3) that CaD ameliorates diabetic nephropathy in a streptozotocin-induced diabetic mouse model by VEGF inhibition. We found that CaD significantly inhibited VEGF165-induced endothelial cell migration, proliferation, and permeability. CaD significantly inhibited VEGF165-induced phosphorylation of VEGFR-2 and suppressed the activity of VEGFR-2 mediated signaling cascades. The effects of CaD in vitro were abrogated by heparin, suggesting the involvement of heparin-like domain in the interaction with CaD. In addition, VEGF121, an isoform which does not bind to heparin, was not inhibited by CaD. By applying proximity ligation assays to endothelial cells, we show inhibition of interaction in situ between HS and VEGF and between VEGF and VEGFR-2. Moreover, CaD reduced VEGF signaling in diabetic kidneys and ameliorated diabetic nephropathy and neuropathy, suggesting CaD as a VEGF inhibitor without the negative effects of complete VEGF blockade and therefore could be useful as a strategy in treating diabetic nephropathy.

cell biology↗

bioRxiv2019

Bacteriophage can promote the emergence of physiologically sub-optimal host phenotypes

Reproduction of bacteria-specific viruses, or bacteriophage, requires the replication and translation machinery of the host cell. As a consequence, phage fitness depends intimately on the physiological state, i.e. growth rate, of the host. We include this dependence of critical phage traits on host growth rate in a mathematical model of a bacteria-phage interaction. This leads to a feedback loop between phage success, host population size, nutrient availability and host growth rate. We find that this feedback allows slow growing bacteria to have a competitive advantage in the presence of phage. Under certain conditions a slow growing host mutant can even drive the phage to extinction. Since in a phage-free environment slow growth is deleterious, the mutant subsequentely dies out as well, constituting a kind of altruistic scenario similar to abortive infections.

ecology↗

bioRxiv2019

Intracellular AIEC LF82 relies on SOS and stringent responses to survive, multiply and tolerate antibiotics.

Adherent Invasive Escherichia coli (AIEC) strains recovered from Crohn's disease lesions survive and multiply within macrophages. A reference strain for this pathovar, AIEC LF82, forms microcolonies within phagolysosomes, an environment that prevents commensal E. coli multiplication. Little is known about the LF82 intracellular growth status, and signals leading to macrophage intra-vacuolar multiplication. We used single-cell analysis, genetic dissection and mathematical models to monitor the growth status and cell cycle regulation of intracellular LF82. We found that within macrophages, bacteria may replicate or undergo non-growing phenotypic switches. This switch results from stringent response firing immediately after uptake by macrophages or at later stages, following genotoxic damage and SOS induction during intracellular replication. Importantly, non-growers resist treatment with various antibiotics. Thus, intracellular challenges induce AIEC LF82 phenotypic heterogeneity and non-growing bacteria that could provide a reservoir for antibiotic-tolerant bacteria responsible for relapsing infections.

microbiology↗

bioRxiv2018

Suicidal Red Queen: Population dynamics and genetic drift accelerate diversity loss

BackgroundRed Queen dynamics are defined as long term co-evolutionary dynamics, often with oscillations of genotype abundances driven by fluctuating selection in host-parasite systems. Much of our current understanding of these dynamics is based on theoretical concepts explored in mathematical models that are mostly (i) deterministic, inferring an infinite population size and (ii) evolutionary, thus ecological interactions that change population sizes are excluded. Here, we recall the different mathematical approaches used in the current literature on Red Queen dynamics. We then compare models from game theory (evo) and classical theoretical ecology models (eco-evo), that are all derived from individual interactions and are thus intrinsically stochastic. We assess the influence of this stochasticity through the time to the first loss of a genotype within a host or parasite population. ResultsThe time until the first genotype is lost ("extinction time"), is shorter when ecological dynamics, in the form of a changing population size, is considered. Furthermore, when individuals compete only locally with other individuals extinction is even faster. On the other hand, evolutionary models with a fixed population size and competition on the scale of the whole population prolong extinction and therefore stabilise the oscillations. The stabilising properties of intraspecific competitions become stronger when population size is increased and the deterministic part of the dynamics gain influence. In general, the loss of genotype diversity can be counteracted with mutations (or recombination), which then allow the populations to recurrently undergo negative frequency-dependent selection dynamics and selective sweeps. ConclusionAlthough the models we investigated are equal in their biological motivation and interpretation, they have diverging mathematical properties both in the derived deterministic dynamics and the derived stochastic dynamics. We find that models that do not consider intraspecific competition and that include ecological dynamics by letting the population size vary, lose genotypes - and thus Red Queen oscillations - faster than models with competition and a fixed population size.

evolutionary biology↗