Carcass Scavenging Relaxes Chemical-Driven Female Interference Competition in Flour Beetles.

AbstractFemale-female nonsexual interference competition is a major fitness determinant of biased sex ratio groups with high female density. What strategies can females use to overcome the negative impact of this competition? To answer this question we used flour beetles (Tribolium castaneum) where competing females from female-biased groups were already known to suppress each other's fecundity by secreting toxic quinones from their stink glands, indicating a unique chemical-driven interference competition. Surprisingly, increasing resources did not alleviate these fitness costs. Females also did not disperse more from the site of interference competition. Hence, the competition was influenced by neither the total resource availability nor the lack of opportunity to avoid chemical interference. Instead, protein sequestered via scavenging of nutrient-rich carcasses relaxed female competition by increasing fecundity and reducing the quinone content. Finally, stink gland components themselves triggered carcass scavenging and increased fecundity, indicating the possibility of a novel chemical-driven feedback loop to reduce the competition. In the present work we provide the rare analyses where multiple competing hypotheses were jointly tested to establish carcass scavenging as an important potential strategy to overcome the fitness costs of intrasexual female interference competition.

Evolution of pathogen tolerance and emerging infections: A missing experimental paradigm.

Researchers worldwide are repeatedly warning us against future zoonotic diseases resulting from humankind's insurgence into natural ecosystems. The same zoonotic pathogens that cause severe infections in a human host frequently fail to produce any disease outcome in their natural hosts. What precise features of the immune system enable natural reservoirs to carry these pathogens so efficiently? To understand these effects, we highlight the importance of tracing the evolutionary basis of pathogen tolerance in reservoir hosts, while drawing implications from their diverse physiological and life-history traits, and ecological contexts of host-pathogen interactions. Long-term co-evolution might allow reservoir hosts to modulate immunity and evolve tolerance to zoonotic pathogens, increasing their circulation and infectious period. Such processes can also create a genetically diverse pathogen pool by allowing more mutations and genetic exchanges between circulating strains, thereby harboring rare alive-on-arrival variants with extended infectivity to new hosts (i.e., spillover). Finally, we end by underscoring the indispensability of a large multidisciplinary empirical framework to explore the proposed link between evolved tolerance, pathogen prevalence, and spillover in the wild.