Figure 2.

Hypothesized pathways in which nongenetic and genetic variation might affect the capacity of populations to evolve in response to the costs of chronically elevated glucocorticoids. Each colored box corresponds to the generation (“light red” = “F₀”; “light green” = “F1”; and “light orange” = “>F2”). “Yellow” dots signify GC concentrations within each fish. (A) Hypothetical situation where sensitized HPA responses (in the absence of genetic variation) are likely to be propagated across generations through nongenetic inheritance (e.g., epigenetic, behavioral propagation, etc.), such that the sensitivity of HPA axis is increased, leading to lifetime fitness costs (inset graph in F1 generation). Such effects are predicted to lead to population decline as populations are caught in a “Non-genetic Trap” (O’Dea et al., 2016). (B) Genetic and nongenetic (epigenetic) variation impacting variation in key factors involved in HPA responses (i.e., glucocorticoid/mineralocorticoid receptor density and affinities, variation in binding globulins, and GC response curves) result in some individuals being less sensitive to thermal stressors (Meylan et al., 2012; Taborsky et al., 2021). Small inset burgundy-filled curves are GC response curves for each fish. The height of each curve for each fish represents the maximal GC response and the width the clearance time of GC’s. Selection in F₀, results in the F₁ population evolving to exhibit different glucocorticoid responses such that variants controlling the expression of GC traits with reduced fitness are selected against (“dashed” parts of lines in F₁ inset). Natural selection may also act on the HPA axis to promote adaptive plasticity or endocrine flexibility (sensu Zimmer et al. 2018), which could be driven by genetic or nongenetic mechanisms (i.e., epigenetic modifications). Changes in GC plastic responses in the F1 generation is predicted to result in lower peak responses and/or faster clearance times.