Figure 1.

Major processes involved in the transition from the undefended to defended phenotype: 1) toxin intake, here visualized with two discrete points representing low and high rates; 2) toxin elimination rate (Elim. Rate), e.g., via toxin metabolism; 3) toxin sequestration rate (Seq. Rate), i.e., the active transport of toxins for storage in a specific location such as the skin; and 4) toxin accumulation rate (Acc. Rate), or the rate at which toxins are accumulated in the animal. Defense phenotypes are ultimately a result of how these processes interact over time, here arbitrarily from 0 h, immediately after toxin ingestion, to 24 h following ingestion. Although toxin intake influences the total possible amount of toxin accumulation, it cannot fully explain the defensive phenotype. We hypothesize that the “no accumulation” phenotype is characterized by the absence of any ability to sequester toxins in combination with a high rate of elimination, resulting in 0 toxin accumulation (solid grey lines); this phenotype is a likely ancestral state for many animals. In contrast, we hypothesize that “passive accumulation” is characterized by lower elimination rates than the no accumulation phenotype, leading to a low amount of toxin accumulation (solid yellow lines); however, some mechanisms of toxin transport could also exist, in which case a low sequestration rate could result in a passive accumulation phenotype when elimination rate is high (dashed yellow lines). We hypothesize that the “active sequestration” phenotype evolves from an intermediate passive accumulation phenotype through the addition of novel sequestration mechanisms that result in high sequestration rates (solid purple lines). However, elimination rates could still modulate the amount of toxins ultimately accumulated, with lower elimination rates resulting in a higher proportion of toxin accumulation overall (dashed purple lines).