Delicate plasticity: Maladaptive responses to fish predation risk in Daphnia magna caused by sertraline pollution

Abstract

An emerging environmental pollutant may have a greater impact on phenotypic plasticity than its direct toxicity, causing maladaptive responses of organisms to their current environment. To better understand such ecological risks, we proposed a delicate plasticity hypothesis: if an emerging stressor acts on the fundamental processes underlying a specific adaptive plastic response, it is more likely to pose high risks to the phenotypic plasticity. Endocrine regulation is one of the critical processes of plasticity and is becoming a target for emerging pollutants. To test this hypothesis, we measured individual traits and the expression of endocrine-related genes in Daphnia magna in response to fish predation risk under exponentially increasing concentrations of the antidepressant sertraline, a selective serotonin reuptake inhibitor. The results showed that sertraline impaired most of the defense responses of D. magna at concentrations lower than the effective concentrations of its direct toxicity. The high risks of sertraline on inducible defenses were also visually reflected in the relationships between toxicity and plasticity strength, that is, most of the defense responses exponentially decayed with an increase in sertraline toxicity. In addition, the expression of genes involved in serotonin synthesis was significantly correlated with the expression of other endocrine-related genes and with changes in morphological traits. These results revealed that environmental sertraline pollution could disturb endocrine regulation and cause high risks to inducible defenses of D. magna, providing evidence supporting the delicate plasticity hypothesis.