Imazethapyr disrupts plant phosphorus homeostasis and acquisition strategies

Abstract

The deficiency of essential mineral nutrients caused by xenobiotics often results in plant mortality or an inability to complete its life cycle. Imazethapyr, a widely utilized imidazolinone herbicide, has a long-lasting presence in the soil-plant system and can induce toxicity in non-target plants. However, the effects of imazethapyr on mineral nutrient homeostasis remain poorly comprehended. In this study, Arabidopsis seedlings exposed to concentrations of 4 and 10 μg/L imazethapyr showed noticeable reductions in shoot development and displayed a distinct dark purple color, which is commonly associated with phosphorus (P) deficiency in crops. Additionally, the total P content in both the shoots and roots of Arabidopsis significantly decreased following imazethapyr treatment when compared to the control groups. Through the complementary use of physiological and molecular analyses, we discovered that imazethapyr hinders the abundance and functionality of inorganic phosphorus (Pi) transporters and acid phosphatase. Furthermore, imazethapyr impairs the plant's Pi-deficiency adaptation strategies, such as inhibiting Pi transporter activities and impeding root hair development, which ultimately exacerbate P starvation. These results provide compelling evidence that residues of imazethapyr have the potential to disrupt plant P homeostasis and acquisition strategies. These findings offer valuable insights for risk assessment and highlight the need to reconsider the indiscriminate use of imazethapyr, particularly under specific scenarios such as nutrient deficiency.