Adaptive strategies of a model diatom Phaeodactylum tricornutum under atrazine exposure.
Diatoms, the core contributors to marine primary productivity, are threatened by rising concentrations of triazine herbicides. However, whether and how diatoms could adapt to such stress remains unclear. Here, we experimentally examined the physiological and metabolic responses of a model diatom species Phaeodactylum tricornutum to atrazine under short-term (∼50 generations) and long-term (∼920 generations) selection. Under short-term exposure, cells sustained their energy supply via ubiquitin‑proteasome‑mediated protein degradation, leading to a temporary increase in tolerance to atrazine; however, this process was accompanied by oxidative stress and cell cycle arrest at the G₂/M phase. After long-term exposure, the population showed heritable tolerance accompanied by coordinated transcriptomic, metabolomic, enzymatic, and physiological changes. And these changes were consistent with enhanced cyclic electron transport, putative malate/oxaloacetate-mediated redox balancing and photorespiration, and coordinated modulation of the oxidative pentose phosphate pathway and fatty acid metabolism. Nevertheless, such tolerance acquisition under long-term exposure incurred phenotypic trade‑offs, including reduced cell size and decreased particulate organic carbon/nitrogen (POC/PON) content, thereby impairing the ecosystem services provided by diatoms. This study indicates that diatoms could develop long-term tolerance to triazine herbicide stress through a two-phase response strategy, with systemic cross-organellar energy coordination (chloroplast-mitochondria crosstalk) and redox-balancing metabolic cycling serving as the coordinated physiological processes underlying heritable tolerance.