Landscape Features Fail to Explain Spatial Genetic Structure in White-Tailed Deer Across Ohio,USA

Landscape features influence wildlife movements across spatial scales and have the potential to influence the spread of disease. Chronic wasting disease (CWD) is a fatal prion disease affecting members of the family Cervidae, particularly white-tailed deer (Odocoileus virginianus), and the first positive CWD case in a wild deer in Ohio, USA, was recorded in 2020. Landscape genetics approaches are increasingly used to better understand potential pathways for CWD spread in white-tailed deer, but little is known about genetic structure of white-tailed deer in Ohio. The objectives of our study were to evaluate spatial genetic structure in white-tailed deer across Ohio and compare the support for isolation by distance (IBD) and isolation by landscape resistance (IBR) models in explaining this structure. We collected genetic data from 619 individual deer from 24 counties across Ohio during 2007–2009. We used microsatellite genotypes from 619 individuals genotyped at 11 loci and haplotypes from a 547-base pair fragment of the mitochondrial DNA control region. We used spatial and non-spatial genetic clustering tests to evaluate genetic structure in both types of genetic data and empirically optimized landscape resistance surfaces to compare IBD and IBR using microsatellite data. Non-spatial genetic clustering tests failed to detect spatial genetic structure, whereas spatial genetic clustering tests indicated subtle spatial genetic structure. The IBD model consistently outperformed IBR models that included land cover, traffic volume, and streams. Our results indicated widespread genetic connectivity of white-tailed deer across Ohio and negligible effects of landscape features. These patterns likely reflect some combination of minimal resistive effects of landscape features on white-tail deer movement in Ohio and the effects of regional recolonization or translocation. We encourage continued CWD surveillance in Ohio, particularly in the proximity of confirmed cases. © 2021 The Wildlife Society. This article has been contributed to by US Government employees and their work is in the public domain in the USA.     

Microbial community transcriptional patterns vary in response to mesoscale forcing in the North Pacific Subtropical Gyre

The physical and biological dynamics that influence phytoplankton communities in the oligotrophic ocean are complex, changing across broad temporal and spatial scales. Eukaryotic phytoplankton (e.g., diatoms), despite their relatively low abundance in oligotrophic waters, are responsible for a large component of the organic matter flux to the ocean interior. Mesoscale eddies can impact both microbial community structure and function, enhancing primary production and carbon export, but the mechanisms that underpin these dynamics are still poorly understood. Here, mesoscale eddy influences on the taxonomic diversity and expressed functional profiles of surface communities of microeukaryotes and particle-associated heterotrophic bacteria from the North Pacific Subtropical Gyre were assessed over 2 years (spring 2016 and summer 2017). The taxonomic diversity of the microeukaryotes significantly differed by eddy polarity (cyclonic versus anticyclonic) and between sampling seasons/years and was significantly correlated with the taxonomic diversity of particle-associated heterotrophic bacteria. The expressed functional profile of these taxonomically distinct microeukaryotes varied consistently as a function of eddy polarity, with cyclones having a different expression pattern than anticyclones, and between sampling seasons/years. These data suggest that mesoscale forcing, and associated changes in biogeochemistry, could drive specific physiological responses in the resident microeukaryote community, independent of species composition.     

Projected climate impacts to South African maize and wheat production in 2055: a comparison of empirical and mechanistic modeling approaches

Crop model‐specific biases are a key uncertainty affecting our understanding of climate change impacts to agriculture. There is increasing research focus on intermodel variation, but comparisons between mechanistic (MMs) and empirical models (EMs) are rare despite both being used widely in this field. We combined MMs and EMs to project future (2055) changes in the potential distribution (suitability) and productivity of maize and spring wheat in South Africa under 18 downscaled climate scenarios (9 models run under 2 emissions scenarios). EMs projected larger yield losses or smaller gains than MMs. The EMs’ median‐projected maize and wheat yield changes were ?3.6% and 6.2%, respectively, compared to 6.5% and 15.2% for the MM. The EM projected a 10% reduction in the potential maize growing area, where the MM projected a 9% gain. Both models showed increases in the potential spring wheat production region (EM = 48%, MM = 20%), but these results were more equivocal because both models (particularly the EM) substantially overestimated the extent of current suitability. The substantial water‐use efficiency gains simulated by the MMs under elevated CO₂ accounted for much of the EM?MM difference, but EMs may have more accurately represented crop temperature sensitivities. Our results align with earlier studies showing that EMs may show larger climate change losses than MMs. Crop forecasting efforts should expand to include EM?MM comparisons to provide a fuller picture of crop–climate response uncertainties.     

Altered Lipid Metabolism in Residual White Adipose Tissues of Bscl2 Deficient Mice

Mutations in BSCL2 underlie human congenital generalized lipodystrophy type 2 disease. We previously reported that Bscl2 ^−/− mice develop lipodystrophy of white adipose tissue (WAT) due to unbridled lipolysis. The residual epididymal WAT (EWAT) displays a browning phenotype with much smaller lipid droplets (LD) and higher expression of brown adipose tissue marker proteins. Here we used targeted lipidomics and gene expression profiling to analyze lipid profiles as well as genes involved in lipid metabolism in WAT of wild-type and Bscl2^−/− mice. Analysis of total saponified fatty acids revealed that the residual EWAT of Bscl2^−/− mice contained a much higher proportion of oleic_18:1n9 acid concomitant with a lower proportion of palmitic_16:0 acid, as well as increased n3- polyunsaturated fatty acids (PUFA) remodeling. The acyl chains in major species of triacylglyceride (TG) and diacylglyceride (DG) in the residual EWAT of Bscl2^−/− mice were also enriched with dietary fatty acids. These changes could be reflected by upregulation of several fatty acid elongases and desaturases. Meanwhile, Bscl2^−/− adipocytes from EWAT had increased gene expression in lipid uptake and TG synthesis but not de novo lipogenesis. Both mitochondria and peroxisomal β-oxidation genes were also markedly increased in Bscl2^−/− adipocytes, highlighting that these machineries were accelerated to shunt the lipolysis liberated fatty acids through uncoupling to dissipate energy. The residual subcutaneous white adipose tissue (ScWAT) was not browning but displays similar changes in lipid metabolism. Overall, our data emphasize that, other than being essential for adipocyte differentiation, Bscl2 is also important in fatty acid remodeling and energy homeostasis.     

Surfactant Protein A Binds Flagellin Enhancing Phagocytosis and IL-1β Production

Surfactant protein A (SP-A), a pulmonary collectin, plays a role in lung innate immune host defense. In this study the role of SP-A in regulating the inflammatory response to the flagella of Pseudomonas aeruginosa (PA) was examined. Intra-tracheal infection of SP-A deficient (SP-A-/-) C57BL/6 mice with wild type flagellated PA (PAK) resulted in an increase in inflammatory cell recruitment and increase in pro-inflammatory cytokines IL-6 and TNF-α, which was not observed with a mutant pseudomonas lacking flagella (fliC). SP-A directly bound flagellin, via the N-linked carbohydrate moieties and collagen-like domain, in a concentration dependent manner and enhanced macrophage phagocytosis of flagellin and wild type PAK. IL-1β was reduced in the lungs of SP-A-/- mice following PAK infection. MH-s cells, a macrophage cell line, generated greater IL-1β when stimulated with flagellin and SP-A. Historically flagella stimulate IL-1β production through the toll-like receptor 5 (TLR-5) pathway and through a caspase-1 activating inflammasome pathway. IL-1β expression became non-detectable in SP-A and flagellin stimulated MH-s cells in which caspase-1 was silenced, suggesting SP-A induction of IL-1β appears to be occurring through the inflammasome pathway. SP-A plays an important role in the pathogenesis of PA infection in the lung by binding flagellin, enhancing its phagocytosis and modifying the macrophage inflammatory response.     

A Liposomal Drug Platform Overrides Peptide Ligand Targeting to a Cancer Biomarker,Irrespective of Ligand Affinity or Density

One method for improving cancer treatment is the use of nanoparticle drugs functionalized with targeting ligands that recognize receptors expressed selectively by tumor cells. In theory such targeting ligands should specifically deliver the nanoparticle drug to the tumor, increasing drug concentration in the tumor and delivering the drug to its site of action within the tumor tissue. However, the leaky vasculature of tumors combined with a poor lymphatic system allows the passive accumulation, and subsequent retention, of nanosized materials in tumors. Furthermore, a large nanoparticle size may impede tumor penetration. As such, the role of active targeting in nanoparticle delivery is controversial, and it is difficult to predict how a targeted nanoparticle drug will behave in vivo. Here we report in vivo studies for α_vβ₆-specific H2009.1 peptide targeted liposomal doxorubicin, which increased liposomal delivery and toxicity to lung cancer cells in vitro. We systematically varied ligand affinity, ligand density, ligand stability, liposome dosage, and tumor models to assess the role of active targeting of liposomes to α_vβ₆. In direct contrast to the in vitro results, we demonstrate no difference in in vivo targeting or efficacy for H2009.1 tetrameric peptide liposomal doxorubicin, compared to control peptide and no peptide liposomes. Examining liposome accumulation and distribution within the tumor demonstrates that the liposome, and not the H2009.1 peptide, drives tumor accumulation, and that both targeted H2009.1 and untargeted liposomes remain in perivascular regions, with little tumor penetration. Thus H2009.1 targeted liposomes fail to improve drug efficacy because the liposome drug platform prevents the H2009.1 peptide from both actively targeting the tumor and binding to tumor cells throughout the tumor tissue. Therefore, using a high affinity and high specificity ligand targeting an over-expressed tumor biomarker does not guarantee enhanced efficacy of a liposomal drug. These results highlight the complexity of in vivo targeting.