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Key message <p><b>Chemically similar metal(loid)s exploit nutrient transport systems and destabilize integrated metal-homeostasis networks, triggering redox imbalance, transcriptional reprogramming, and multiscale regulatory responses that ultimately determine plant adaptation or toxicity.</b></p> Abstract <p>Plant growth depends on the homeostasis of mineral nutrients, but it is short in heterogeneous soils where required elements are found together with chemically similar harmful metal(loid)s. The divalent ionic and coordination properties of Cd–Zn and Ni–Fe are similar, while the arsenate–phosphate interactions are structurally analogous oxyanion mimicry systems. Cd–Zn, Ni–Fe, and As–P have broad-substrate transport systems with partially overlapping ion-recognition properties, notably under nutrient-limiting conditions. Although it is widely recognized that transporter promiscuity exists in a systemic manner. The overall systemic effects, such as metal homeostasis, redox signaling, activity of the organelles, transcriptional regulation, and whole-plant ion balance between tissues and cellular compartments of its action, are not yet clearly understood. We are stating that chemically similar metal stress signifies the destabilization of an integrated homeostatic network and not just limitation of transporters. Substantial overlap exists in conserved transporter families (ZIP, NRAMP, PHT, IRT, HMA), which are triggered by nutritional deprivation to induce high-affinity transporter families, which stimulates the uptake of both essential and simultaneously detrimental metals. Competitive metal entry causes disruption of the cytosolic and organellar redox balance, leading to the production of ROS, which results in transcriptional reprogramming, turnover of transporters, metal redistribution, and calcium-, kinase-, and hormone-mediated signaling. In addition to uptake, intracellular regulatory mechanisms act to control metal partitioning, including thiol chelation, vacuolar sequestration, metallochaperone activity, organelle-specific redistribution, and transporter dynamics. Root exudation and plant–microbe interactions are some of the rhizospheric activities that cause further speciation of the metals before they can enter the membrane. We suggest a multiscale model, in which coordinated regulatory reprogramming during co-exposure is the basis for adaptive resistance, and failure of metal homeostasis, and redox-feedback regulation is the basis for toxicity. Chemical mimicry can therefore be considered a systemic limitation of the productivity of plants.</p>

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Transporter promiscuity and redox-driven metal partitioning in plant responses to chemically analogous metals

  • 期刊论文

  • 发表日期：

    2026年6月22日

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  • Sudhir Kumar Upadhyay

摘要

Key message

Chemically similar metal(loid)s exploit nutrient transport systems and destabilize integrated metal-homeostasis networks, triggering redox imbalance, transcriptional reprogramming, and multiscale regulatory responses that ultimately determine plant adaptation or toxicity.

Abstract

Plant growth depends on the homeostasis of mineral nutrients, but it is short in heterogeneous soils where required elements are found together with chemically similar harmful metal(loid)s. The divalent ionic and coordination properties of Cd–Zn and Ni–Fe are similar, while the arsenate–phosphate interactions are structurally analogous oxyanion mimicry systems. Cd–Zn, Ni–Fe, and As–P have broad-substrate transport systems with partially overlapping ion-recognition properties, notably under nutrient-limiting conditions. Although it is widely recognized that transporter promiscuity exists in a systemic manner. The overall systemic effects, such as metal homeostasis, redox signaling, activity of the organelles, transcriptional regulation, and whole-plant ion balance between tissues and cellular compartments of its action, are not yet clearly understood. We are stating that chemically similar metal stress signifies the destabilization of an integrated homeostatic network and not just limitation of transporters. Substantial overlap exists in conserved transporter families (ZIP, NRAMP, PHT, IRT, HMA), which are triggered by nutritional deprivation to induce high-affinity transporter families, which stimulates the uptake of both essential and simultaneously detrimental metals. Competitive metal entry causes disruption of the cytosolic and organellar redox balance, leading to the production of ROS, which results in transcriptional reprogramming, turnover of transporters, metal redistribution, and calcium-, kinase-, and hormone-mediated signaling. In addition to uptake, intracellular regulatory mechanisms act to control metal partitioning, including thiol chelation, vacuolar sequestration, metallochaperone activity, organelle-specific redistribution, and transporter dynamics. Root exudation and plant–microbe interactions are some of the rhizospheric activities that cause further speciation of the metals before they can enter the membrane. We suggest a multiscale model, in which coordinated regulatory reprogramming during co-exposure is the basis for adaptive resistance, and failure of metal homeostasis, and redox-feedback regulation is the basis for toxicity. Chemical mimicry can therefore be considered a systemic limitation of the productivity of plants.