The Dynamics of a Metapopulation: Changes in Life-History Traits in Resident Herring that Co-Occur with Oceanic Herring during Spawning

Different populations of Atlantic herring are regarded as forming a metapopulation, but we know little about the dynamics of the connectivity and degree of interbreeding between the populations. Based on data from three periods between 1962 and 2011, we identified the presence of two components of herring in a small semi-enclosed coastal marine ecosystem based on different somatic growth patterns and mean vertebrae sum (VS). The two components were interpreted as belonging to a resident herring population and the migratory, oceanic Norwegian spring spawning (NSS) herring population, and they co-occurred during spawning. In the 1960s, resident herring characterized by slow growth and low VS co-occurred with rapid growth, high VS oceanic NSS herring. Similar slow-growing resident and rapid-growing NSS herring were found in the 1970–80s, but both populations now had low VS suggesting similar origins. Finally, in the 2000s both populations showed rapid growth. The changes coincided with the NSS herring going from a state of high abundance and oceanic distribution to a collapse in the late 1960s that resulted in a coastal distribution closer to resident herring populations, before full recovery and resumption of the migratory, oceanic pattern in the 1990s. During all three periods, NSS herring were only present in the local system up to an age of about five years, but the synchronous spawning of the populations supports mixed spawning and interbreeding. During the investigation period both longevity, length at age (growth) and length-at-first maturity increased markedly for the resident herring, which then became more similar to the NSS herring. Genetic and/or cultural factors are believed to be the main causes of the observed changes in life history traits, although some effect of changes in environmental factors cannot be excluded. Our study suggests that relationships among populations in a metapopulation can be highly dynamic.     

Review: predatory soil mites as biocontrol agents of above- and below-ground plant pests

Biological pest control is becoming increasingly important for sustainable agriculture. Although many species of natural enemies are already being used commercially, efficient biological control of various pests is still lacking, and there is a need for more biocontrol agents. In this review, we focus on predatory soil mites, their role as natural enemies, and their biocontrol potential, mainly in vegetable and ornamental crops, with an emphasis on greenhouse systems. These predators are still underrepresented in biological control, but have several advantages compared to predators living on above-ground plant parts. For example, predatory soil mites are often easy and affordable to mass rear, as most of them are generalist predators, which also means that they may be used against various pests and can survive periods of pest scarcity by feeding on alternative prey or food. Many of them can also endure unfavourable conditions, making it easier for them to establish in various crops. Based on the current literature, we show that they have potential to control a variety of pests, both in greenhouses and in the field. However, more research is needed to fully understand and appreciate their potential as biocontrol agents. We review and discuss several methods to increase their efficiency, such as supplying them with alternative food and changing soil/litter structure to enable persistence of their populations. We conclude that predatory soil mites deserve more attention in future studies to increase their application in agricultural crops.

     

Exercise during pregnancy mitigates Alzheimer-like pathology in mouse offspring

Physical activity protects brain function in healthy individuals and those with Alzheimer's disease (AD). Evidence for beneficial effects of parental exercise on the health status of their progeny is sparse and limited to nondiseased individuals. Here, we questioned whether maternal running interferes with offspring's AD-like pathology and sought to decipher the underlying mechanisms in TgCRND8 mice. Maternal stimulation was provided by voluntary wheel running vs. standard housing during pregnancy. Following 5 mo of standard housing of transgenic and wild-type offspring, their brains were examined for AD-related pathology and/or plasticity changes. Running during pregnancy reduced β-amyloid (Aβ) plaque burden (-35%, P=0.017) and amyloidogenic APP processing in transgenic offspring and further improved the neurovascular function by orchestrating different Aβ transporters and increasing angiogenesis (+29%, P=0.022). This effect was accompanied by diminished inflammation, as indicated by reduced microgliosis (-20%, P=0.002) and down-regulation of other proinflammatory mediators, and resulted in less oxidative stress, as nitrotyrosine levels declined (-28%, P=0.029). Moreover, plasticity changes (in terms of up-regulation of reelin, synaptophysin, and ARC) were found not only in transgenic but also in wild-type offspring. We conclude that exercise during pregnancy provides long-lasting protection from neurodegeneration and improves brain plasticity in the otherwise unstimulated progeny.     

Sex allocation in relation to host races in the brood-parasitic common cuckoo (Cuculus canorus)

Sex allocation theory and empirical evidence both suggest that natural selection should favour maternal control of offspring sex ratio in relation to their ability to invest in the offspring. Generalist parasites constitute a particularly interesting group to test this theory as different females commonly utilize different host species showing large variation in provisioning ability. The common cuckoo (Cuculus canorus) is a generalist brood parasite that lays its eggs in the nest of many different passerine birds, but each female tends to specialize on one particular host species giving rise to highly specialized host races. The different host species show large variation in their ability to invest in the parasitic offspring, presenting an opportunity for female cuckoos to bias offspring sex ratio in relation to host species quality. Here, we investigate host-race specific sex allocation controlling for maternal identity in the common cuckoo. We found no evidence of any significant relationship between host race and sex ratio in one sympatric population harbouring three different host races, or in a total of five geographically separated populations. There was also no significant association between host quality, as determined by species-specific female host body mass, and cuckoo sex ratio. Finally, we found no significant relationship between individual cuckoo maternal quality, as determined by her egg volume, and sex ratio within each host race. We conclude that the generalist brood-parasitic common cuckoo show no significant sex-ratio bias in relation to host race and discuss this finding in light of gene flow and host adaptations.     

Tree mineral nutrition is deteriorating in Europe

The response of forest ecosystems to increased atmospheric CO₂ is constrained by nutrient availability. It is thus crucial to account for nutrient limitation when studying the forest response to climate change. The objectives of this study were to describe the nutritional status of the main European tree species, to identify growth‐limiting nutrients and to assess changes in tree nutrition during the past two decades. We analysed the foliar nutrition data collected during 1992–2009 on the intensive forest monitoring plots of the ICP Forests programme. Of the 22 significant temporal trends that were observed in foliar nutrient concentrations, 20 were decreasing and two were increasing. Some of these trends were alarming, among which the foliar P concentration in F. sylvatica, Q. Petraea and P. sylvestris that significantly deteriorated during 1992–2009. In Q. Petraea and P. sylvestris, the decrease in foliar P concentration was more pronounced on plots with low foliar P status, meaning that trees with latent P deficiency could become deficient in the near future. Increased tree productivity, possibly resulting from high N deposition and from the global increase in atmospheric CO₂, has led to higher nutrient demand by trees. As the soil nutrient supply was not always sufficient to meet the demands of faster growing trees, this could partly explain the deterioration of tree mineral nutrition. The results suggest that when evaluating forest carbon storage capacity and when planning to reduce CO₂ emissions by increasing use of wood biomass for bioenergy, it is crucial that nutrient limitations for forest growth are considered.     

siRNA knock down of glutamate dehydrogenase in astrocytes affects glutamate metabolism leading to extensive accumulation of the neuroactive amino acids glutamate and aspartate

Glutamate is the most abundant excitatory neurotransmitter in the brain and astrocytes are key players in sustaining glutamate homeostasis. Astrocytes take up the predominant part of glutamate after neurotransmission and metabolism of glutamate is necessary for a continuous efficient removal of glutamate from the synaptic area. Glutamate may either be amidated by glutamine synthetase or oxidatively metabolized in the mitochondria, the latter being at least to some extent initiated by oxidative deamination by glutamate dehydrogenase (GDH). To explore the particular importance of GDH for astrocyte metabolism we have knocked down GDH in cultured cortical astrocytes employing small interfering RNA (siRNA) achieving a reduction of the enzyme activity by approximately 44%. The astrocytes were incubated for 2h in medium containing either 1.0mM [(15)NH(4)(+)] or 100μM [(15)N]glutamate. For those exposed to [(15)N]glutamate an additional 100μM was added after 1h. Metabolic mapping was performed from isotope incorporation measured by mass spectrometry into relevant amino acids of cell extracts and media. The contents of the amino acids were measured by HPLC. The (15)N incorporation from [(15)NH(4)(+)] into glutamate, aspartate and alanine was decreased in astrocytes exhibiting reduced GDH activity. However, the reduced GDH activity had no effect on the cellular contents of these amino acids. This supports existing in vivo and in vitro studies that GDH is predominantly working in the direction of oxidative deamination and not reductive amination. In contrast, when exposing the astrocytes to [(15)N]glutamate, the reduced GDH activity led to an increased (15)N incorporation into glutamate, aspartate and alanine and a large increase in the content of glutamate and aspartate. Surprisingly, this accumulation of glutamate and net-synthesis of aspartate were not reflected in any alterations in either the glutamine content or labeling, but a slight increase in mono labeling of glutamine in the medium. We suggest that this extensive net-synthesis of aspartate due to lack of GDH activity is occurring via the concerted action of AAT and the part of TCA cycle operating from α-ketoglutarate to oxaloacetate, i.e. the truncated TCA cycle.     

Endoplasmic reticulum stress response promotes cytotoxic phenotype of CD8αβ+ intraepithelial lymphocytes in a mouse model for Crohn's disease-like ileitis

Endoplasmic reticulum (ER) unfolded protein responses (UPR) are implicated in the pathogenesis of inflammatory bowel disease. Cytotoxic CD8αβ(+) intraepithelial lymphocytes (IEL) contribute to the development of Crohn's disease-like ileitis in TNF(ΔARE/+) mice. In this study, we characterized the role of ER-UPR mechanisms in contributing to the disease-associated phenotype of cytotoxic IEL under conditions of chronic inflammation. Inflamed TNF(ΔARE/+) mice exhibited increased expression of Grp78, ATF6, ATF4, and spliced XBP1 in CD8αβ(+) IEL but not in CD8αα(+) IEL or in lamina propria lymphocytes. Chromatin immunoprecipitation analysis in CD8αβ(+) T cells showed selective recruitment of ER-UPR transducers to the granzyme B gene promoter. Heterozygous Grp78(-/+) mice exhibited an attenuated granzyme B-dependent cytotoxicity of CD8αβ(+) T cells against intestinal epithelial cells, suggesting a critical activity of this ER-associated chaperone in maintaining a cytotoxic T cell phenotype. Granzyme B-deficient CD8αβ(+) T cells showed a defect in IL-2-mediated proliferation in Grp78(-/+) mice. Adoptively transferred Grp78(-/+) CD8αβ(+) T cells had a decreased frequency of accumulation in the intestine of RAG2(-/-) recipient mice. The tissue pathology in TNF(ΔARE/+) × Grp78(-/+) mice was similar to TNF(ΔARE/+) mice, even though the cytotoxic effector functions of CD8αβ(+) T cells were significantly reduced. In conclusion, ER stress-associated UPR mechanisms promote the development and maintenance of the pathogenic cytotoxic CD8αβ(+) IEL phenotype in the mouse model of Crohn's disease-like ileitis.     

Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 Deficiency Reduces Insulin Sensitivity in High-Fat Diet-Fed Mice

Adipose tissue inflammation is considered an important contributor to insulin resistance. Mitogen-activated protein kinase-activated protein kinase 2 (MK2) is a major downstream target of p38 MAPK and enhances inflammatory processes. In line with the role of MK2 as contributor to inflammation, MK2^−/− mice are protected against inflammation in different disease models. Therefore, MK2 is considered an attractive therapeutic target for the treatment of chronic inflammatory diseases. This study tested the impact of MK2-deficiency on high-fat diet (HFD)-induced adipose tissue inflammation and insulin resistance. After feeding MK2^−/− and WT control mice a HFD (60% energy from fat) for 24 weeks, body weight was not different between groups. Also, liver weight and the amount of abdominal fat remained unchanged. However, in MK2^−/− mice plasma cholesterol levels were significantly increased. Surprisingly, macrophage infiltration in adipose tissue was not altered. However, adipose tissue macrophages were more skewed to the inflammatory M1 phenotype in MK2^−/− mice. This differerence in macrophage polarization did however not translate in significantly altered expression levels of Mcp-1, Tnfα and Il6. Glucose and insulin tolerance tests demonstrated that MK2^−/− mice had a significantly reduced glucose tolerance and increased insulin resistance. Noteworthy, the expression of the insulin-responsive glucose transporter type 4 (GLUT4) in adipose tissue of MK2^−/− mice was reduced by 55% (p<0.05) and 33% (p<0.05) on the mRNA and protein level, respectively, compared to WT mice. In conclusion, HFD-fed MK2^−/− display decreased glucose tolerance and increased insulin resistance compared to WT controls. Decreased adipose tissue expression of GLUT4 might contribute to this phenotype. The data obtained in this study indicate that clinical use of MK2 inhibitors has to be evaluated with caution, taking potential metabolic adverse effects into account.     

The Homeostatic Chemokine CCL21 Predicts Mortality in Aortic Stenosis Patients and Modulates Left Ventricular Remodeling

Background

CCL21 acting through CCR7, is termed a homeostatic chemokine. Based on its role in concerting immunological responses and its proposed involvement in tissue remodeling, we hypothesized that this chemokine could play a role in myocardial remodeling during left ventricular (LV) pressure overload.

Methods and Results

Our main findings were: (i) Serum levels of CCL21 were markedly raised in patients with symptomatic aortic stenosis (AS, n = 136) as compared with healthy controls (n = 20). (ii) A CCL21 level in the highest tertile was independently associated with all-cause mortality in these patients. (iii) Immunostaining suggested the presence of CCR7 on macrophages, endothelial cells and fibroblasts within calcified human aortic valves. (iv). Mice exposed to LV pressure overload showed enhanced myocardial expression of CCL21 and CCR7 mRNA, and increased CCL21 protein levels. (v) CCR7^−/− mice subjected to three weeks of LV pressure overload had similar heart weights compared to wild type mice, but increased LV dilatation and reduced wall thickness.

Conclusions

Our studies, combining experiments in clinical and experimental LV pressure overload, suggest that CCL21/CCR7 interactions might be involved in the response to pressure overload secondary to AS.