Climate change reduces extent of temperate drylands and intensifies drought in deep soils

Drylands cover 40% of the global terrestrial surface and provide important ecosystem services. While drylands as a whole are expected to increase in extent and aridity in coming decades, temperature and precipitation forecasts vary by latitude and geographic region suggesting different trajectories for tropical, subtropical, and temperate drylands. Uncertainty in the future of tropical and subtropical drylands is well constrained, whereas soil moisture and ecological droughts, which drive vegetation productivity and composition, remain poorly understood in temperate drylands. Here we show that, over the twenty first century, temperate drylands may contract by a third, primarily converting to subtropical drylands, and that deep soil layers could be increasingly dry during the growing season. These changes imply major shifts in vegetation and ecosystem service delivery. Our results illustrate the importance of appropriate drought measures and, as a global study that focuses on temperate drylands, highlight a distinct fate for these highly populated areas

Differential regulation of cell motility and invasion by FAK

Cell migration and invasion are fundamental components of tumor cell metastasis. Increased focal adhesion kinase (FAK) expression and tyrosine phosphorylation are connected with elevated tumorigenesis. Null mutation of FAK results in embryonic lethality, and FAK−/− fibroblasts exhibit cell migration defects in culture. Here we show that viral Src (v-Src) transformation of FAK−/− cells promotes integrin-stimulated motility equal to stable FAK reexpression. However, FAK−/− v-Src cells were not invasive, and FAK reexpression, Tyr-397 phosphorylation, and FAK kinase activity were required for the generation of an invasive cell phenotype. Cell invasion was linked to transient FAK accumulation at lamellipodia, formation of a FAK–Src-p130Cas–Dock180 signaling complex, elevated Rac and c-Jun NH2-terminal kinase activation, and increased matrix metalloproteinase expression and activity. Our studies support a dual role for FAK in promoting cell motility and invasion through the activation of distinct signaling pathways

Skeletal muscle munc18c and syntaxin 4 in human obesity

<p>Abstract</p> <p>Background</p> <p>Animal and cell culture data suggest a critical role for Munc18c and Syntaxin 4 proteins in insulin mediated glucose transport in skeletal muscle, but no studies have been published in humans.</p> <p>Methods</p> <p>We investigated the effect of a 12 vs. 48 hr fast on insulin action and skeletal muscle Munc18c and Syntaxin 4 protein in lean and obese subjects. Healthy lean (n = 14; age = 28.0 +/- 1.4 yr; BMI = 22.8 +/- 0.42 kg/m²) and obese subjects (n = 11; age = 34.6 +/- 2.3 yr; BMI = 36.1 +/- 1.5 kg/m²) were studied twice following a 12 and 48 hr fast. Skeletal muscle biopsies were obtained before a 3 hr 40 mU/m²/min hyperinsulinemic-euglycemic clamp with [6,6-²H₂]glucose infusion.</p> <p>Results</p> <p>Glucose rate of disappearance (Rd) during the clamp was lower in obese vs. lean subjects after the 12 hr fast (obese: 6.25 +/- 0.67 vs. lean: 9.42 +/- 1.1 mg/kgFFM/min, p = 0.007), and decreased significantly in both groups after the 48 hr fast (obese 3.49 +/- 0.31 vs. lean: 3.91 +/- 0.42 mg/kgFFM/min, p = 0.002). Munc18c content was not significantly different between lean and obese subjects after the 12 hour fast, and decreased after the 48 hr fast in both groups (p = 0.013). Syntaxin 4 content was not altered by obesity or fasting duration. There was a strong positive relationship between plasma glucose concentration and Munc18c content in lean and obese subjects during both 12 and 48 hr fasts (R²= 0.447, p = 0.0015). Significant negative relationships were also found between Munc18c and FFA (p = 0.041), beta-hydroxybutyrate (p = 0.039), and skeletal muscle AKT content (p = 0.035) in lean and obese subjects.</p> <p>Conclusion</p> <p>These data indicate Munc18c and Syntaxin 4 are present in human skeletal muscle. Munc18c content was not significantly different between lean and obese subjects, and is therefore unlikely to explain obesity-induced insulin resistance. Munc18c content decreased after prolonged fasting in lean and obese subjects concurrently with reduced insulin action. These data suggest changes in Munc18c content in skeletal muscle are associated with short-term changes in insulin action in humans.</p

Humanized Mice Recapitulate Key Features of HIV-1 Infection: A Novel Concept Using Long-Acting Anti-Retroviral Drugs for Treating HIV-1

BACKGROUND: Humanized mice generate a lymphoid system of human origin subsequent to transplantation of human CD34+ cells and thus are highly susceptible to HIV infection. Here we examined the efficacy of antiretroviral treatment (ART) when added to food pellets, and of long-acting (LA) antiretroviral compounds, either as monotherapy or in combination. These studies shall be inspiring for establishing a gold standard of ART, which is easy to administer and well supported by the mice, and for subsequent studies such as latency. Furthermore, they should disclose whether viral breakthrough and emergence of resistance occurs similar as in HIV-infected patients when ART is insufficient. METHODS/PRINCIPAL FINDINGS: NOD/shi-scid/γ(c)null (NOG) mice were used in all experimentations. We first performed pharmacokinetic studies of the drugs used, either added to food pellets (AZT, TDF, 3TC, RTV) or in a LA formulation that permitted once weekly subcutaneous administration (TMC278: non-nucleoside reverse transcriptase inhibitor, TMC181: protease inhibitor). A combination of 3TC, TDF and TMC278-LA or 3TC, TDF, TMC278-LA and TMC181-LA suppressed the viral load to undetectable levels in 15/19 (79%) and 14/14 (100%) mice, respectively. In successfully treated mice, subsequent monotherapy with TMC278-LA resulted in viral breakthrough; in contrast, the two LA compounds together prevented viral breakthrough. Resistance mutations matched the mutations most commonly observed in HIV patients failing therapy. Importantly, viral rebound after interruption of ART, presence of HIV DNA in successfully treated mice and in vitro reactivation of early HIV transcripts point to an existing latent HIV reservoir. CONCLUSIONS/SIGNIFICANCE: This report is a unique description of multiple aspects of HIV infection in humanized mice that comprised efficacy testing of various treatment regimens, including LA compounds, resistance mutation analysis as well as viral rebound after treatment interruption. Humanized mice will be highly valuable for exploring the antiviral potency of new compounds or compounds targeting the latent HIV reservoir

Differential Ligand Binding to a Human Cytomegalovirus Chemokine Receptor Determines Cell Type–Specific Motility

While most chemokine receptors fail to cross the chemokine class boundary with respect to the ligands that they bind, the human cytomegalovirus (HCMV)-encoded chemokine receptor US28 binds multiple CC-chemokines and the CX3C-chemokine Fractalkine. US28 binding to CC-chemokines is both necessary and sufficient to induce vascular smooth muscle cell (SMC) migration in response to HCMV infection. However, the function of Fractalkine binding to US28 is unknown. In this report, we demonstrate that Fractalkine binding to US28 not only induces migration of macrophages but also acts to inhibit RANTES-mediated SMC migration. Similarly, RANTES inhibits Fractalkine-mediated US28 migration in macrophages. While US28 binding of both RANTES and Fractalkine activate FAK and ERK-1/2, RANTES signals through Gα12 and Fractalkine through Gαq. These findings represent the first example of differential chemotactic signaling via a multiple chemokine family binding receptor that results in migration of two different cell types. Additionally, the demonstration that US28-mediated chemotaxis is both ligand-specific and cell type–specific has important implications in the role of US28 in HCMV pathogenesis

Communal roosting sites are potential ecological traps: experimental evidence in a Neotropical harvestman

Situations in which animals preferentially settle in low-quality habitat are referred to as ecological traps, and species that aggregate in response to conspecific cues, such as scentmarks, that persist after the animals leave the areamay be especially vulnerable. We tested this hypothesis on harvestmen (Prionostemma sp.) that roost communally in the rainforest understory. Based on evidence that these animals preferentially settle in sites marked with conspecific scent, we predicted that established aggregation sites would continue to attract new recruits even if the animals roosting there perished. To test this prediction, we simulated intense predation by repeatedly removing all individuals from 10 established roosts, and indeed, these sites continued to attract new harvestmen. A more likely reason for an established roost to become unsuitable is a loss of overstory canopy cover caused by treefalls. To investigate this scenario, without felling trees, we established 16 new communal roosts by translocating harvestmen into previously unused sites. Half the release sites were located in intact forest, and half were located in treefall gaps, but canopy cover had no significant effect on the recruitment rate. These results support the inference that communal roost sites are potential ecological traps for species that aggregate in response to conspecific scent

DrylandEcology/rSW2exter: v0.2.1

fetch_mukeys_spatially_NRCS_SDA() now requires at least "soilDB" version 2.6.10 (and no longer supports "sp"; @dschlaep). Linting updated to lintr >= 3.1 (@dschlaep). Full Changelog: https://github.com/DrylandEcology/rSW2exter/compare/v0.2.0...v0.2.

Why only tetraploid Solidago gigantea (Asteraceae) became invasive: A common garden comparison of ploidy levels

ISSN:0029-8549ISSN:1432-193

Data from: Genetic effects of anthropogenic habitat fragmentation on remnant animal and plant populations: a meta-analysis

Habitat loss and fragmentation are among the biggest threats to biodiversity. Anthropogenic habitat fragmentation leads to small and isolated remnant plant and animal populations. The combination of increased random genetic drift, inbreeding, and reduced gene flow may substantially reduce genetic variation of remnant populations. However, the magnitude of these responses may depend on several poorly understood factors including organism group, habitat type of both the fragment and the surrounding matrix, life‐history traits, and time since fragmentation. We compiled data for 83 plant and 52 animal species and conducted a meta‐analysis following best practices to evaluate how these factors mediate the effects of anthropogenic habitat fragmentation. We calculated 206 effect sizes as correlations between one of four measures of population‐level genetic diversity and fragment area. All analyses were repeated using models of increasing complexity (traditional random‐effects models, multilevel models accounting for non‐independent data, and multilevel models additionally correcting for phylogenetic relatedness). We confirmed that anthropogenic habitat fragmentation has overall negative effects on genetic diversity of organisms. Our meta‐analysis shows, however, that plant species responded in general stronger to fragmentation than animal species and that the largest negative impacts of fragmentation occurred in tropical and temperate forest fragments, surrounded by a non‐forest matrix. In contrast, we found only weak responses in non‐forest fragments. Genetic diversity measured as mean number of alleles (A) showed the strongest response to fragmentation. Expected heterozygosity (He) and percentage of polymorphic loci (PLP) showed similar but weaker responses. In contrast, our meta‐analysis indicated that inbreeding (Fis) was not measurably affected by anthropogenic habitat fragmentation. Additionally, our models revealed that effects on genetic diversity became stronger with age of fragments: We found significant negative responses for fragments older than 50 yr but not for those more recently isolated. Our meta‐analyses also showed that currently animals are underrepresented in the literature on genetic effects of anthropogenic fragmentation, as are certain geographical regions and habitat types. We expect that future field studies using state‐of‐the‐art approaches will provide further evidence of negative genetic effects, which may reinforce the here reported patterns, even for groups not yet studied