Mineral nutrient acquisition under stress: Sensing, signaling, and transportation.

Plants commonly face abiotic stressors like drought, salinity, and limited nutrient availability which disrupt the homeostatic networks of mineral acquisition and hamper productivity. In this review we aim to clarify the molecular platforms by which plants sense and act in response to fluctuating availability of nitrogen and phosphorus under stress. Our data show that the dual-affinity nitrate transporter NRT1.1 functions as a sensor and transporter, controlling root architecture and downstream signaling through the TOR-NLP7-SnRK1 pathway to modulate nitrate homeostasis under water and nutrient stress. NRT1.1 activity is also modulated by abscisic acid (ABA) via the PP2C-type phosphatase ABI2, which regulates its phosphorylation status and thereby its nitrate transport capacity. This highlights a direct point of integration between ABA and nitrogen signaling (Leran et al., 2015). Perception of phosphorus is also controlled through the PHR1-SPX module: with Pi availability in excess, SPX proteins suppress PHR1 activity; However, under Pi-deficient conditions, this inhibition is lifted, allowing PHR1 to induce the expression of PHT1 phosphate transporters and miR399, which mediates systemic phosphate remobilization by targeting PHO2 (Puga et al., 2014; Duan et al., 2008). This PHR1-SPX interaction has been experimentally validated using yeast two-hybrid (Y2H) assays, co-immunoprecipitation, and reporter gene analysis, confirming the direct physical interaction under high Pi availability (Puga et al., 2014). Along with nutrient-specific pathways, our data reveal strong interactions between hormonal signaling, reactive oxygen species (ROS), and calcium signaling. Drought-induced ABA accumulation modulates NRT1.1 expression and synchronizes nitrogen uptake with water status; ethylene signaling under low Pi availability enhances root hair growth for acquisition of phosphate; and ROS bursts under nutrient deficiency activate calcium-dependent protein kinases (CDPKs) and MAPKs to modulate transporter stability with precision. Oscillations in calcium, sensed by CBL-CIPK complexes, integrate multiple stress signals further to modulate ion channels (e.g., AKT1 for potassium uptake) and transcriptional networks. Lastly, we describe biotechnological innovations, specifically CRISPR-Cas9 genome editing and nanotechnology-capable of enhancing nutrient-use efficiency and stress tolerance. Targeted editing of OsNPF3.1 and OsHAK8 alleles illustrates how CRISPR can enhance nitrogen and potassium uptake under stressful conditions, while new nanofertilizers (like ZnO and Si nanoparticles) and ROS-scavenging nanomaterials designed for mitigation of oxidative stress provide targeted, slow-release avenues for micronutrient delivery and protection from oxidative damage. They combine to elucidate how NRT1.1 and PHR1-SPX modules, as enhanced by hormone-ROS-Ca²⁺ cross-signaling, regulate stress nutrient acquisition. They also provide the potential to use CRISPR and nanotechnology-based approaches to grow more nutrient-use-efficient and abiotic stress-tolerant plants.