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Abstract Litter decomposition is one of the largest carbon (C) fluxes in terrestrial ecosystems and links aboveground biomass to soil C pools. In grasslands, decomposition drivers have received substantial attention but the role of grassland herbivores in influencing decay rates is often ignored despite their potentially large effects on standing biomass and nutrient cycling. Recent work has demonstrated that nutrient addition increases early-stage decay and suppresses late-stage decay. Mammalian herbivores can mediate the effects of nutrient supply on biomass, suggesting herbivores may alter the effects of nutrients on decomposition, though this is largely unknown. We examined how herbivory mediates the effects of nutrient supply on long-term decomposition across 19 grassland sites of the Nutrient Network distributed experiment. At each site, a full-factorial experiment of combined nitrogen (N), phosphorus (P), and micronutrient (K) enrichment (‘control’ or ‘ + NPK’) and mammalian herbivore (> ~ 50 g) exclusion (‘unfenced’ or ‘fenced’) was carried out in a randomized block design. We hypothesized that nutrient effects on litter decomposition would be strongest where herbivores caused the greatest reductions in aboveground plant biomass (i.e., at sites with more intense herbivory). After accounting for wide variation in decomposition rates across sites, we found that, within sites, elevated nutrients increased early-stage decay and suppressed late-stage decay. In contrast, neither herbivore exclusion (i.e., fencing) nor site level changes in aboveground biomass due to herbivory altered the nutrient effects on decomposition rates. Across grasslands, our results indicate that elevated nutrient supply modifies litter decomposition rates independent of herbivore impacts. 

Abstract Researchers have long sought to understand and predict an animal’s response to stressful stimuli. Since the introduction of the concept of homeostasis, a variety of model frameworks have been proposed to describe what is necessary for an animal to remain within this stable physiological state and the ramifications of leaving it. Romero et al. (Horm Behav 55(3):375–389, 2009) introduced the reactive scope model to provide a novel conceptual framework for the stress response that assumes an animal’s ability to tolerate a stressful stimulus may degrade over time in response to the stimulus. We provide a mathematical formulation for the reactive scope model using a system of ordinary differential equations and show that this model is capable of recreating existing experimental data. We also provide an experimental method that may be used to verify the model as well as several potential additions to the model. If future experimentation provides the necessary data to estimate the model’s parameters, the model presented here may be used to make quantitative predictions about physiological mediator levels during a stress response and predict the onset of homeostatic overload. 

By dispersing seeds long distances, large, fruit-eating animals influence plant population spread and community dynamics. After fruit consumption, animal gut passage time and movement determine seed dispersal patterns and distances. These, in turn, are influenced by extrinsic, environmental variables and intrinsic, individual-level variables. We simulated seed dispersal by forest elephants ( Loxodonta cyclotis ) by integrating gut passage data from wild elephants with movement data from 96 individuals. On average, elephants dispersed seeds 5.3 km, with 89% of seeds dispersed farther than 1 km. The longest simulated seed dispersal distance was 101 km, with an average maximum dispersal distance of 40.1 km. Seed dispersal distances varied among national parks, perhaps due to unmeasured environmental differences such as habitat heterogeneity and configuration, but not with human disturbance or habitat openness. On average, male elephants dispersed seeds farther than females. Elephant behavioral traits strongly influenced dispersal distances, with bold, exploratory elephants dispersing seeds 1.1 km farther than shy, idler elephants. Protection of forest elephants, particularly males and highly mobile, exploratory individuals, is critical to maintaining long distance seed dispersal services that shape plant communities and tropical forest habitat. 

Rationale: There is incomplete knowledge of the impact of bone marrow cells on the gut microbiome and gut barrier function. Objective: We postulated that diabetes mellitus and systemic ACE2 (angiotensin-converting enzyme 2) deficiency would synergize to adversely impact both the microbiome and gut barrier function. Methods and Results: Bacterial 16S rRNA sequencing and metatranscriptomic analysis were performed on fecal samples from wild-type, ACE2 −/y , Akita (type 1 diabetes mellitus), and ACE2 −/y -Akita mice. Gut barrier integrity was assessed by immunofluorescence, and bone marrow cell extravasation into the small intestine was evaluated by flow cytometry. In the ACE2 −/y -Akita or Akita mice, the disrupted barrier was associated with reduced levels of myeloid angiogenic cells, but no increase in inflammatory monocytes was observed within the gut parenchyma. Genomic and metatranscriptomic analysis of the microbiome of ACE2 −/y -Akita mice demonstrated a marked increase in peptidoglycan-producing bacteria. When compared with control cohorts treated with saline, intraperitoneal administration of myeloid angiogenic cells significantly decreased the microbiome gene expression associated with peptidoglycan biosynthesis and restored epithelial and endothelial gut barrier integrity. Also indicative of diabetic gut barrier dysfunction, increased levels of peptidoglycan and FABP-2 (intestinal fatty acid-binding protein 2) were observed in plasma of human subjects with type 1 diabetes mellitus (n=21) and type 2 diabetes mellitus (n=23) compared with nondiabetic controls (n=23). Using human retinal endothelial cells, we determined that peptidoglycan activates a noncanonical TLR-2 (Toll-like receptor 2) associated MyD88 (myeloid differentiation primary response protein 88)-ARNO (ADP-ribosylation factor nucleotide-binding site opener)-ARF6 (ADP-ribosylation factor 6) signaling cascade, resulting in destabilization of p120-catenin and internalization of VE-cadherin as a mechanism of deleterious impact of peptidoglycan on the endothelium. Conclusions: We demonstrate for the first time that the defect in gut barrier function and dysbiosis in ACE2 −/y -Akita mice can be favorably impacted by exogenous administration of myeloid angiogenic cells.