Editorial: Ecosystem Services and Disservices Provided by Plant-Feeding Predatory Arthropods

n/

The Zoophytophagous Predator Macrolophus pygmaeus Induces Tomato Resistance against Spider Mites

Many predatory insects that prey on herbivores also feed on the plant, but it is unknown whether plants affect the performance of herbivores by responding to this phytophagy with defence induction. We investigate whether the prior presence of the omnivorous predator Macrolophus pygmaeus (Rambur) on tomato plants affects plant resistance against two different herbivore species. Besides plant-mediated effects of M. pygmaeus on herbivore performance, we examined whether a plant defence trait that is known to be inducible by herbivory, proteinase inhibitors (PI), may also be activated in response to the interactions of this predator with the tomato plant. We show that exposing tomato plants to the omnivorous predator M. pygmaeus reduced performance of a subsequently infesting herbivore, the two-spotted spider mite Tetranychus urticae Koch, but not of the greenhouse whitefly Trialeurodes vaporariorum (Westwood). The spider-mite infested tomato plants experience a lower herbivore load, i.e., number of eggs deposited and individuals present, when previously exposed to the zoophytophagous predator. This effect is not restricted to the exposed leaf and persists on exposed plants for at least two weeks after the removal of the predators. The decreased performance of spider mites as a result of prior exposure of the plant to M. pygmaeus is accompanied by a locally and systemically increased accumulation of transcripts and activity of proteinase inhibitors that are known to be involved in plant defence. Our results demonstrate that zoophytophagous predators can induce plant defence responses and reduce herbivore performance. Hence, the suppression of populations of certain herbivores via consumption may be strengthened by the induction of plant defences by zoophytophagous predators

Pollen Provisioning Enhances the Performance of Amblydromalus limonicus on an Unsuitable Prey

Amblydromalus limonicus is a polyphagous phytoseiid predator used for the biological control of thrips and whiteflies in greenhouse crops. Besides various prey species, A. limonicus can also feed on pollen of different plants. Cattail pollen has been previously shown to be suitable for the development and reproduction of A. limonicus. Hence, it could sustain its populations in periods of prey scarcity. In the present study, we hypothesized that pollen provisioning may benefit A. limonicus in mixed diets with prey of low quality, such as spider mites and thus, positively impact ecosystem services provided by this predator. For this, the performance and predation efficiency of A. limonicus against spider mites was assessed in the presence or absence of pollen. Our results show that pollen significantly shortens the developmental time and increases the survival and oviposition of the predator when mixed with spider mites, although it negatively affects its predation rate. Nevertheless, pollen enhances the maintenance of juvenile predators on the leaf by substantially decreasing their dispersal rate in the mixed diet with spider mites. In addition, the intrinsic rate of population increase (rm) of A. limonicus feeding with spider mites increased with the addition of pollen suggesting an increase in its population. Cattail pollen as supplementary food may thus expand the prey species range that A. limonicus could exploit. It can also enhance ecosystem services provided against other pests (thrips and whiteflies) by positively affecting the increase of A. limonicus population

Alcohol Affects the Brain's Resting-State Network in Social Drinkers

Acute alcohol intake is known to enhance inhibition through facilitation of GABAA receptors, which are present in 40% of the synapses all over the brain. Evidence suggests that enhanced GABAergic transmission leads to increased large-scale brain connectivity. Our hypothesis is that acute alcohol intake would increase the functional connectivity of the human brain resting-state network (RSN). To test our hypothesis, electroencephalographic (EEG) measurements were recorded from healthy social drinkers at rest, during eyes-open and eyes-closed sessions, after administering to them an alcoholic beverage or placebo respectively. Salivary alcohol and cortisol served to measure the inebriation and stress levels. By calculating Magnitude Square Coherence (MSC) on standardized Low Resolution Electromagnetic Tomography (sLORETA) solutions, we formed cortical networks over several frequency bands, which were then analyzed in the context of functional connectivity and graph theory. MSC was increased (p<0.05, corrected with False Discovery Rate, FDR corrected) in alpha, beta (eyes-open) and theta bands (eyes-closed) following acute alcohol intake. Graph parameters were accordingly altered in these bands quantifying the effect of alcohol on the structure of brain networks; global efficiency and density were higher and path length was lower during alcohol (vs. placebo, p<0.05). Salivary alcohol concentration was positively correlated with the density of the network in beta band. The degree of specific nodes was elevated following alcohol (vs. placebo). Our findings support the hypothesis that short-term inebriation considerably increases large-scale connectivity in the RSN. The increased baseline functional connectivity can -at least partially- be attributed to the alcohol-induced disruption of the delicate balance between inhibitory and excitatory neurotransmission in favor of inhibitory influences. Thus, it is suggested that short-term inebriation is associated, as expected, to increased GABA transmission and functional connectivity, while long-term alcohol consumption may be linked to exactly the opposite effect

Eight Americas: Investigating Mortality Disparities across Races, Counties, and Race-Counties in the United States

BACKGROUND: The gap between the highest and lowest life expectancies for race-county combinations in the United States is over 35 y. We divided the race-county combinations of the US population into eight distinct groups, referred to as the “eight Americas,” to explore the causes of the disparities that can inform specific public health intervention policies and programs. METHODS AND FINDINGS: The eight Americas were defined based on race, location of the county of residence, population density, race-specific county-level per capita income, and cumulative homicide rate. Data sources for population and mortality figures were the Bureau of the Census and the National Center for Health Statistics. We estimated life expectancy, the risk of mortality from specific diseases, health insurance, and health-care utilization for the eight Americas. The life expectancy gap between the 3.4 million high-risk urban black males and the 5.6 million Asian females was 20.7 y in 2001. Within the sexes, the life expectancy gap between the best-off and the worst-off groups was 15.4 y for males (Asians versus high-risk urban blacks) and 12.8 y for females (Asians versus low-income southern rural blacks). Mortality disparities among the eight Americas were largest for young (15–44 y) and middle-aged (45–59 y) adults, especially for men. The disparities were caused primarily by a number of chronic diseases and injuries with well-established risk factors. Between 1982 and 2001, the ordering of life expectancy among the eight Americas and the absolute difference between the advantaged and disadvantaged groups remained largely unchanged. Self-reported health plan coverage was lowest for western Native Americans and low-income southern rural blacks. Crude self-reported health-care utilization, however, was slightly higher for the more disadvantaged populations. CONCLUSIONS: Disparities in mortality across the eight Americas, each consisting of millions or tens of millions of Americans, are enormous by all international standards. The observed disparities in life expectancy cannot be explained by race, income, or basic health-care access and utilization alone. Because policies aimed at reducing fundamental socioeconomic inequalities are currently practically absent in the US, health disparities will have to be at least partly addressed through public health strategies that reduce risk factors for chronic diseases and injuries

Bi-allelic variants in NAE1 cause intellectual disability, ischiopubic hypoplasia, stress-mediated lymphopenia and neurodegeneration

Neddylation has been implicated in various cellular pathways and in the pathophysiology of numerous diseases. We identified four individuals with bi-allelic variants in NAE1, which encodes the neddylation E1 enzyme. Pathogenicity was supported by decreased NAE1 abundance and overlapping clinical and cellular phenotypes. To delineate how cellular consequences of NAE1 deficiency would lead to the clinical phenotype, we focused primarily on the rarest phenotypic features, based on the assumption that these would best reflect the pathophysiology at stake. Two of the rarest features, neuronal loss and lymphopenia worsening during infections, suggest that NAE1 is required during cellular stress caused by infections to protect against cell death. In support, we found that stressing the proteasome system with MG132—requiring upregulation of neddylation to restore proteasomal function and proteasomal stress—led to increased cell death in fibroblasts of individuals with NAE1 genetic variants. Additionally, we found decreased lymphocyte counts after CD3/CD28 stimulation and decreased NF-κB translocation in individuals with NAE1 variants. The rarest phenotypic feature—delayed closure of the ischiopubic rami—correlated with significant downregulation of RUN2X and SOX9 expression in transcriptomic data of fibroblasts. Both genes are involved in the pathophysiology of ischiopubic hypoplasia. Thus, we show that NAE1 plays a major role in (skeletal) development and cellular homeostasis during stress. Our approach suggests that a focus on rare phenotypic features is able to provide significant pathophysiological insights in diseases caused by mutations in genes with pleiotropic effects.</p