Larval Performance of a Major Forest Pest on Novel Hosts and the Effect of Stressors

Novel hosts lacking a coevolutionary history with herbivores can often support improved larval performance over historic hosts; e.g., emerald ash borer [Agrilus planipennis (Fairmaire) Coleoptera: Buprestidae] on North American ash (Fraxinus spp.) trees. Whether trees are novel or ancestral, stress on plants increases emerald ash borer preference and performance. White fringetree [Chionanthus virginicus (L.) Lamiales: Oleaceae] and olive [Olea europaea (L.) Lamiales: Oleaceae] are closely related non-ash hosts that support development of emerald ash borer to adulthood, but their relative suitability as hosts and the impact of plant stress on larval success has not been well studied. In a series of experiments, survival and growth of emerald ash borer larvae on these novel hosts were examined along with the impact of stress. In the first experiment, larvae grew more slowly in cut stems of olive than in green ash [Fraxinus pennsylvanica (Marshall) Lamiales: Oleaceae] and several adults successfully emerged from larger olive stems. In two experiments on young potted olive with photosynthesizing bark, larvae died within a week, but mechanical girdling increased the rate of gallery establishment. The final two experiments on field-grown fringetrees found increased larval survivorship and growth in previously emerald ash borer attacked and mechanically girdled plants than in healthy stems or stems treated with the defense hormone, methyl jasmonate. Our results demonstrate that these non-ash hosts are less suitable for emerald ash borer than preferred ash hosts, but previous emerald ash borer attack or girdling led to better survival and growth demonstrating the importance of stress for larval success. In potted olive, high mortality could be due to higher loads of toxic compounds or the presence of chlorophyllous tissue.

Transgenerational effects of ancestral prenatal stress on the gut-brain axis

The effects of ancestral prenatal stress can propagate across generations to alter the well-being of directly and indirectly exposed descendants via epigenetic mechanisms. Prenatal stress has been shown to alter the function of the gut-brain axis, a bi-directional signaling pathway between the gut microbiome and the enteric and central nervous systems. There has been no study investigating the impact of remote prenatal stress in ancestors on the gut-microbiome connection. Here we investigated if exposure to transgenerational ancestral stress affects the gut-brain axis through changes in the microbiome and microbiota. A multigenerational rat cohort consisting of a F0, F1, F2, and F3 generation was utilized in this study. Pregnant dams in the F0 generation were exposed to repeated restraint stress and overnight social isolation from gestational days 12-18. Breeding of three successive generations occurred in the absence of gestational stress along with a lineage of yoked controls. Fecal collection occurred for males and female in each generation at the age of 30 days, 90 days, and 115 days. Fecal samples were analyzed using 1H-NMR spectroscopy to examine the metabolome. The data are being analysed using supervised and unsupervised machine learning approaches. The data are expected to reveal that the fecal metabolome is characteristically altered by ancestral prenatal stress in each generation, resulting in a biomarker signature that is linked to the behavioural phenotype. We predict changes in the gut metabolome and microbiome to be most significant in the F3 generation. These findings could lead to further understanding of intestinal dysbiosis and its impact on the brain, and sex-specific metabolic biomarkers that are predictive of stress-associated adverse health outcomes.

Stress-Induced Evolutionary Innovation: A Mechanism for the Origin of Cell Types

Understanding the evolutionary role of environmentally-induced phenotypic variation (i.e., environmental plasticity) is an important issue in developmental evolution. One of the major physiological responses to environmental changes is cellular stress, which is counteracted by a generic stress reaction that detoxifies the cell, refolds proteins, and repairs DNA damage. In this paper, we elaborate on a previous finding suggesting that the cell differentiation cascade of human decidual stromal cells, a cell type critical for embryo implantation and the maintenance of pregnancy, evolved from a cellular stress reaction. We hypothesize that the stress reaction in these cells was elicited ancestrally through the inflammation caused by embryo attachment and invasion. We describe a model, Stress-Induced Evolutionary Innovation (SIEI), whereby ancestral stress reactions and their corresponding pathways can be transformed into novel structural components of body plans, such as new cell types. After reviewing similarities and differences between SIEI and the “plasticity first hypothesis” (PFH) of evolution, we argue that SIEI is a distinct form of plasticity-based evolutionary change because it leads to the origin of novel structures rather than the adaptive transformation of a pre-existing character.