Biology subjects

Hausmann, R.

Publications and source records attributed to Hausmann, R..

7 recordsLinked to original sources

bioRxiv2026

Forest biodiversity benefits from warmer microclimate, but only in colder regions

The diversity of many forest-dwelling organisms depends on forest structure, but it remains unknown to which degree this is mediated by microclimatic temperature, and whether microclimatic buffering is universally beneficial for forest biodiversity. In 234 broad-leaved forest plots across nine climatically differing regions in Germany, we measured micro- and macroclimatic temperatures, canopy cover, and deadwood volume after experimental manipulations of forest structure through thinning operations and gap cuts. We surveyed 21 taxonomic groups, representing plants, bacteria, fungi, and animals, to assess how their diversity depended on the predictors. Multi-taxon diversity, and diversity of ten separate taxonomic groups, increased from closed to open canopies. Only necrophagous beetles were more diverse in closed stands. These effects of canopy cover on diversity were partly mediated by microclimatic temperatures. Thereby, diversity responses to microclimatic temperature depended on the macroclimatic context. In regions with colder summers, locally warmer microclimates in canopy gaps had strong positive effects on biodiversity, while these effects were not found in regions with warmer summers. Consequently, management strategies aimed at multi-taxon forest diversity conservation should be chosen based on the regional climate, favoring canopy gaps primarily in colder regions, and taking future climate warming into consideration.

ecology↗

bioRxiv2026

Sample coverage standardization ranks species richness of saproxylic beetles across European tree genera

Aims In forest ecosystems, tree species composition and diversity are fundamental drivers of biodiversity and many species are closely associated to specific tree species as hosts. Saproxylic diversity across tree species may be shaped by interactions between ecological and environmental factors, such as resource availability. However, a throughout and unbiased quantification of diversity across tree species is missing. We investigated patterns an drivers of saproxylic beetle diversity across European tree genera while accounting for differences in sampling effort. Location Europe Methods We used a large dataset, of 25 studies, comprising 500,000 deadwood-dependent beetles, representing 1041 saproxylic beetle species, sampled from 29 tree genera. We accounted for sampling effort by estimating diversity using coverage-based standardization across Hill numbers. We than used linear models to identify drivers of saproxylic beetle diversity across tree genera and assessed differences in community composition using Nonmetric Multidimensional Scaling (NMDS). Additionally, the most abundant beetle families were identified for a subset of 14 genera. Results Quercus supported the highest richness of infrequent, frequent, and highly frequent species, while Fagus exhibited the highest observed (unstandardized) species richness. Beetle communities were less differentiated when focusing on infrequent species, whereas tree genera were separated when focusing on frequent and highly frequent species. In addition, we found that resource availability and maximum tree height best predicted infrequent beetle diversity, whereas resource availability was the main driver of frequent species. In contrast, the same analyses for unstandardized data indicated postglacial occurrence as an important factor for infrequent species. Main conclusions Although resource availability supported the species area hypothesis, standardized data revealed higher richness on smaller trees, partly contradicting this pattern. Our results highlight the importance of accounting for sampling bias and promoting tree diversity, particularly oaks, to sustain saproxylic beetle diversity.

ecology↗

bioRxiv2026

Outer Pore Collapse as a Potential Mechanism of Partial Loss of Pain in Nav1.7 M899I

Complete loss of function of the voltage-gated sodium channel subtype Nav1.7, encoded by SCN9A, results in congenital insensitivity to pain. Here, we investigate a previously identified variant, M899I, in which methionine at position 899 is substituted by isoleucine. This variant was originally described in a Chinese patient with loss of pain. We confirmed membrane expression of the mutant channel in HEK cells using extracellular HA-tagging; however, no sodium currents were detectable from the variant in patch-clamp recordings. The M899I substitution is located within a tightly packed hydrophobic region of the pore module. Introducing the corresponding variant into Nav1.2 and Nav1.5 similarly abolished channel function, underscoring the high conservation and functional importance of this residue. To further investigate the underlying mechanism, we combined in-silico coarse-grained molecular dynamics simulations with in-vitro electrophysiological analysis. Our simulations predicted that the M899I substitution induces collapse of the outer pore, substantially reducing both pore radius and volume. Substitution with other hydrophobic residues was likewise predicted to alter pore geometry and, consequently, ion permeation to varying degrees. Whole-cell voltage-clamp recordings validated these predictions, with observed current densities closely correlating with the extent of pore collapse predicted in silico. Together, our findings establish pore collapse as a mechanism underlying disease-relevant loss-of-function variants in Nav1.7 and suggest that this principle may extend to other sodium channel subtypes. Moreover, our results demonstrate that in-silico molecular dynamics approaches can reliably predict structural and functional consequences of channel mutations, as confirmed by in-vitro electrophysiological data.

biophysics↗

bioRxiv2025

Higher bat and bird γ-diversity in structurally complex forests is driven by distinct α- and β-diversity responses

Effective conservation management and habitat restoration rely on understanding how biodiversity responds to environmental change. Centuries of silviculture have homogenized forests and their species communities globally, reducing biodiversity. To test whether restoring forest structural complexity can promote biodiversity, we conducted a large-scale, spatially explicit landscape experiment. At 11 sites across Germany, we compared bat and bird diversity in forests with experimentally enhanced heterogeneity by increasing deadwood and canopy complexity to homogeneous production forests. Both taxa were investigated by autonomous acoustic recorders and automatic species identification. We quantified within-patch (-), between-patch ({beta}-), and landscape-level ({gamma}-) diversity, emphasizing infrequent to highly frequent species for taxonomic, functional, and phylogenetic diversity. The pairwise comparisons of the sites were synthesized using a newly developed meta-analysis of rarefaction-extrapolation curves. {gamma}-diversity increased significantly in structurally heterogeneous forests for both taxa, albeit through distinct taxon-specific mechanisms. Bat {gamma}-diversity gains were primarily driven by higher {beta}-diversity, indicating greater dissimilarity in species assemblages among patches, while bird {gamma}-diversity increased via higher -diversity within patches. Bat diversity increases were mainly taxonomic, suggesting functional similarity in the communities, whereas birds showed the highest gains in functional diversity, indicating that experimental treatments resulted in greater trait dissimilarity. Our results provide experimental evidence under real-world conditions that {gamma}-diversity can be shaped by different diversity mechanisms. These patterns likely originate from differences in activity ranges, such as the large-scale movements of foraging bats in contrast to the more spatially restricted, territorial behavior of birds. This highlights the need for taxon-specific restoration strategies in homogenized landscapes.

ecology↗

bioRxiv2025

Better Safe Than Sorry: Leg Amputations as a Prophylactic Wound Care Behaviour in Carpenter Ants

Animals often sustain injuries, which are susceptible to lethal infections. In social insects, wound care behaviours have evolved to reduce these risks. But the limits of wound care behaviours remain unclear. Here we investigated the wound care behaviours of the ant Camponotus maculatus. Our findings show that amputation of legs infected with Pseudomonas aeruginosa significantly reduced mortality. However, nestmates do not differentiate between infected and sterile injuries, providing similar treatments regardless of infection. Even though we show that early amputation correlates with higher survival rates, nestmates amputate indiscriminately on legs with fresh or old wounds. Additionally, cuticular hydrocarbon profiles differed between ants with infected or sterile wounds only 24 hours post-injury, a timepoint when amputations are no longer effective. We propose that C. maculatus workers perform prophylactic amputations regardless of injury state or age. This is in sharp contrast to previous studies which showed clear capabilities to treat infected wounds differently in ants using antimicrobial compounds. This work therefore shows the limits of wound care behaviours in social insects, allowing us to better understand the evolutionary drivers of this unique behaviour.

animal behavior and cognition↗

bioRxiv2022

Diclofenac and other Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) are Competitive Antagonists of the human P2X3 Receptor

The P2X3 receptor (P2X3R), an ATP-gated non-selective cation channel of the P2X receptor family, is expressed in sensory neurons and involved in nociception. P2X3R inhibition was shown to reduce chronic and neuropathic pain. In a previous screening of 2000 approved drugs, natural products and bioactive substances, various non-steroidal anti-inflammatory drugs (NSAIDs) were found to inhibit P2X3R-mediated currents. To investigate whether the inhibition of P2X receptors contributes to the analgesic effect of NSAIDs, we characterized the potency and selectivity of various NSAIDs at P2X3R and other P2XR subtypes using two-electrode voltage clamp electrophysiology. We identified diclofenac as a hP2X3R and hP2X2/3R antagonist with micromolar potency (with IC50 values of 138.2 {micro}M and 76.7 {micro}M, respectively). A weaker inhibition of hP2X1R, hP2X4R and hP2X7R by diclofenac was determined. Flufenamic acid (FFA) proved to inhibit hP2X3R, rP2X3R and hP2X7R (IC50 values of 221{micro}M, 264.1{micro}M and [~] 900{micro}M, respectively), questioning its widespread use as a nonselective ion channel blocker, when P2XR-mediated currents are under study. Inhibition of the hP2X3R or hP2X2/3R by diclofenac could be overcome by prolonged ATP-application or increasing concentrations of the agonist ,{beta}-meATP, respectively, indicating competition of diclofenac and the agonists. Molecular dynamics simulation showed that diclofenac largely overlaps with ATP bound to the open state of the hP2X3R. Our results strongly support a competitive antagonism through which diclofenac, by interacting with residues of the ATP-binding site, left flipper, and dorsal fin domains inhibits gating of P2X3R by conformational fixation of the left flipper and dorsal fin domains. In summary, we demonstrate the inhibition of the human P2X3 receptor by various NSAIDs. Diclofenac proved to be the most effective antagonist with a strong inhibition of hP2X3R and hP2X2/3R and a weaker inhibition of hP2X1R, hP2X4R and hP2X7R. Considering their involvement in nociception, inhibition of hP2X3R and hP2X2/3R by micromolar concentrations of diclofenac may contribute to the analgesic effect as well as the side effect of taste disturbances of diclofenac and represent an additional mode of action besides the well-known high potency COX inhibition.

pharmacology and toxicology↗

bioRxiv2022

Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents

Voltage-gated sodium channels (Nav) are key players in excitable tissues with the capability to generate and propagate action potentials. Mutations in the genes encoding Navs can lead to severe inherited diseases, and some of these so-called channelopathies are showing temperature sensitive phenotypes, for example paramyotonia congenita, Brugada-syndrome, febrile seizure syndromes and inherited pain syndromes like erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD). Nevertheless, most investigations of mutation-induced gating effects were conducted at room temperature and thus the role of cooling or warming in channelopathies remains poorly understood. Here, we investigated the temperature sensitivity of four Nav subtypes: Nav1.3, Nav1.5, Nav1.6, and Nav1.7 and two mutations in Nav1.7 causing IEM (Nav1.7/L823R) and PEPD (Nav1.7/I1461T), using an automated patch clamp system. Our experiments at 15 {degrees}C, 25 {degrees}C and 35 {degrees}C revealed a shift of the voltage dependence of activation to more hyperpolarized potentials with increasing temperature for all investigated subtypes. Nav1.3 exhibited strongly slowed inactivation kinetics compared to the other subtypes that resulted in enhanced persistent current especially at 15 {degrees}C, indicating a possible role in cold induced hyperexcitability. Impaired fast inactivation of Nav1.7/I1461T was significantly enhanced by cooling temperature to 15 {degrees}C. The subtype specific modulation as well as the intensified mutation induced gating changes stress the importance to consider temperature as regulator for channel gating and its impact on cellular excitability as well as disease phenotypes. SummaryActivation of the sodium channel subtypes Nav1.3, Nav1.5, Nav1.6, and Nav1.7 and two pain linked mutations is alleviated by warmth. Cooler temperatures, on the other hand, strongly enhance persistent currents of Nav1.3. The impaired fast inactivation of the pain-linked Nav1.7/I1461T mutation is further impaired by cooling, mimicking clinical findings.

physiology↗