Search

1. Species-rich communities exhibit higher levels of ecosystem functioning compared to species-poor ones, and this positive relationship strengthens over time. One proposed explanation for this phenomenon is the reduction of niche overlap among plants or animals, which corresponds to increased complementarity and reduced competition. 2. In order to examine the potential of increased complementarity among plants or animals to strengthen the relationship between diversity and ecosystem functions, we integrated models of bio-energetic population dynamics and food-web assembly. Through the simulation of various scenarios of plant and animal complementarity change, we sought to elucidate the mechanisms underlying the observed increases in (1) primary productivity, (2) control of herbivores by predators, and (3) reduction of herbivore pressure on plants in species-rich communities. 3. Our findings reveal that increased niche complementarity of plants can steepen the diversity-function relationships if it does not increase their intraspecific competition, while increasing complementarity among animals during community assembly can also have a positive effect but with considerable variability. 4. The study highlights the importance of trait variation both among and within species, and the interplay between intra- and interspecific competition strength in shaping the functioning of ecosystems over time. These results offer insights into the mechanisms underpinning the diversity-functioning relationship, and have practical implications for ecosystem management and conservation efforts.

On a global scale, fisheries harvest an estimated 96 million tonnes of fish biomass annually, making them one of the most important drivers of marine ecosystem biodiversity. Yet little is known about the interactions between fisheries and the dynamics of complex food webs in which the harvested species are embedded. We have developed a synthetic model that combines resource economics with complex food webs to examine the direct effects of fishing on exploited species and the indirect impact on other species in the same community. Our model analyses show that the sensitivity of the targeted species increases with its trophic level and decreases with its local interaction complexity (i.e. its number of interactions with prey, predators, and competitors). In addition, we also document a strikingly positive effect of community species richness on the resilience of the harvested species to this disturbance. The indirect effects on other species show specific patterns of spreading across trophic modules that differ systematically from how other disturbances spread across ecological networks. While these results call for further research on how human resource exploitation in general and fishery in particular affect ecological dynamics and biodiversity in naturally complex systems, they also allow for some cautious conclusions. Taken together, our results suggest that the sustainability concerning fishery yield and ecosystem integrity can be maximised by focusing the harvest on low trophic level species with a high local interaction complexity in high biodiversity ecosystems. In this sense, our complex network approach offers a promising avenue for integrating the necessities of generating economic revenue with the protection of natural biodiversity.

For over a decade, multiple studies have disputed the notion of natural killer (NK) cells as purely innate lymphocytes by demonstrating that they are capable of putative antigen-specific immunological memory against multiple infectious agents including two critical global health priorities – HIV and influenza. However, the mechanisms underlying antigen specificity remain unknown. Herein, we demonstrate that antigen-specific human NK cell memory develops upon exposure to both HIV and influenza, unified by a conserved and epitope-specific targetable mechanism firmly dependent on the activating CD94/NKG2C receptor and its ligand HLA-E, and confirm these findings by three rigorous and novel assays. We validated the permanent acquisition of antigen-specificity by individual memory NK cells by single-cell cloning. We identified biomarkers of antigen-specific NK cell memory through RNA-Seq transcriptomic fingerprints and complex immunophenotyping by 30-parameter flow cytometry showing elevated expression of KLRG1, α4β7 and NKG2C. Finally, we show individual HLA-E-restricted peptides that may constitute the dominant response in HIV-1- and influenza-infected persons in vivo. Our findings clarify the mechanisms behind formation of antigen-specific memory NK cells, and suggest they could be targeted for future vaccines, cure strategies, or other therapeutic interventions.

Human language enables us to externalise self-internal information (e.g. emotions or beliefs that are not readily accessible to others). Thus, language bridges the gap between the self and the other (e.g. Frith and Frith, 2010) in a way that possibly no other communication system can provide. In many languages, the difference between the self and others is directly reflected in the distinction between first (“I”), second (“you”) and third person (“he, she”) marking. In the present study, we compared ERPs to first, second and third person pronouns during the comprehension of an audio-book version of The Little Prince. Our results revealed a strong P300 response following first person pronouns that is independent of contextual factors. In line with previous research on self-relevance and the P300 (e.g. Knolle, Schröger, and Kotz, 2013b), our results suggest that first person marking is an attentional cue for self-relevance that is at the core of successful narrative comprehension. Refereed/Peer-reviewed

The free radical theory of aging is based on the idea that reactive oxygen species (ROS) may lead to the accumulation of age-related protein oxidation. Because themajority of cellular ROS is generated at the respiratory electron transport chain, this study focuses on the mitochondrial proteome of the aging model Podospora anserina as target for ROS-induced damage. To ensure the detection of even low abundant modified peptides, separation by long gradient nLC-ESI-MS/MS and an appropriate statistical workflow for iTRAQ quantification was developed. Artificial protein oxidation was minimized by establishing gel-free sample preparation in the presence of reducing and iron-chelating agents. This first large scale, oxidative modification-centric study for P. anserina allowed the comprehensive quantification of 22 different oxidative amino acid modifications, and notably the quantitative comparison of oxidized and nonoxidized protein species. In total 2341 proteins were quantified. For 746 both protein species (unmodified and oxidatively modified) were detected and the modification sites determined. The data revealed that methionine residues are preferably oxidized. Further prominent identified modifications in decreasing order of occurrence were carbonylation as well as formation of N-formylkynurenine and pyrrolidinone. Interestingly, for the majority of proteins a positive correlation of changes in protein amount and oxidative damage were noticed, and a general decrease in protein amounts at late age. However, it was discovered that few proteins changed in oxidative damage in accordance with former reports. Our data suggest that P. anserina is efficiently capable to counteract ROS-induced protein damage during aging as long as protein de novo synthesis is functioning, ultimately leading to an overall constant relationship between damaged and undamaged protein species. These findings contradict a massive increase in protein oxidation during aging and rather suggest a protein damage homeostasis mechanism even at late age.

Novel influenza vaccine approaches to achieve cross-protection against a broad range of antigenically distinct strains are needed. Beyond their ability to eliminate infected cells without the need for prior sensitization, natural killer (NK) cells have been shown to mediate virus-specific recall responses. Notably, exposure to influenza antigens induces protective influenza-specific memory NK cells in mice, but evidence of influenza-specific memory NK cells in humans is still lacking. Using intracellular cytokine staining, we found that NK cells from 45% of adults can robustly respond to nucleoprotein (NP) from at least 2 heterosubtypic influenza strains completely independent of T cell help. To further determine if a subset of NK cells can specifically react to NP peptide pools from distinct strains, we clonally expanded individual NK cells (NKCL) and measured H1N1, H2N2 and H3N2 NP-specific killing by 33 NKCL from 6 donors. 63% of NKCL showed positive responses against the 2009 H1N1 pandemic strain (2%–57% specific lysis). Strikingly, half of H1N1 NP-specific NKCL also displayed cytotoxicity against either H2N2 or H3N2 (9%–100% specific lysis) or against both H2N2 and H3N2 strains (5%–11% specific lysis). Potent killing by NKCLs was associated with high cell surface expression of the activating NKG2C receptor, a ligand for HLA-E. Accordingly, we identified an HLA-E-restricted NP epitope that triggers activation of influenza-specific NK cells. Collectively, these data provide the first mechanistic evidence of influenza-specific memory NK cells in humans and suggest influenza-specific responses mediated by NK cells may have the potential to be harnessed to enhance influenza vaccine-induced cross-protection.