Low phosphate (Pi) availability and high aluminum (Al) toxicity constitute two major plant mineral nutritional stressors that limit plant productivity on acidic soils. Advances toward the identification of genes and signaling networks that are involved in both stresses in model plants such as Arabidopsis thaliana and rice (Oryza sativa), and in other plants as well have revealed that some factors such as organic acids (OAs), cell wall properties, phytohormones, and iron (Fe) homeostasis are interconnected with each other. Moreover, OAs are involved in recruiting of many plant-growth-promoting bacteria that are able to secrete both OAs and phosphatases to increase Pi availability and decrease Al toxicity. In this review paper, we summarize these mutual mechanisms by which plants deal with both Al toxicity and P starvation, with emphasis on OA secretion regulation, plant-growth-promoting bacteria, transcription factors, transporters, hormones, and cell wall-related kinases in the context of root development and root system architecture remodeling that plays a determinant role in improving P use efficiency and Al resistance on acidic soils.

Soil salinization is increasingly threatening global agricultural productivity and food security, currently affecting over 6% of the world’s land and one-third of irrigated areas. Tomato (Solanum lycopersicum L.), a major vegetable crop worldwide, exhibits moderate sensitivity to salinity, which limits both its yield and fruit quality. In recent years, epigenetic regulation has gained attention as a key mechanism enabling flexible and reversible control of gene expression without altering DNA sequences. This review synthesizes current knowledge on the epigenetic control of salt stress responses in tomato, focusing on three interconnected levels: DNA methylation dynamics, RNA-directed DNA methylation (RdDM), and histone modifications. We explore how DNA methyltransferases reshape the methylome under salinity, using examples such as PKE1 and SlGI to illustrate functional gene-body methylation. The RdDM pathway is discussed with emphasis on the unexpected role of SlAGO4A as a negative modulator of stress tolerance and the growing evidence for RdDM-mediated regulation of transcription factors. We also examine the balanced regulation of histone acetylation and deacetylation, highlighting the conserved role of GCN5 in maintaining cell wall integrity and the diverse functions of histone deacetylases, such as SlHDA1, SlHDA3, and SlHDA5, in stress adaptation. Additionally, insights from wild tomato species and grafting-induced epigenetic changes are presented, revealing new dimensions of stress memory. Collectively, these epigenetic mechanisms constitute a complex regulatory framework that integrates stress responses with growth and development, providing potential targets for epigenetic breeding of salt-tolerant tomatoes.

Nitrate fertilizers exacerbate Fe deficiency in plants, a phenomenon traditionally attributed to rhizosphere alkalinization that reduces Fe bioavailability. However, whether nitrate itself acts as a signaling molecule in this process has remained unclear. Here, we demonstrate that nitrate functions as an essential signaling molecule that regulates Fe deficiency responses in Arabidopsis through NLP7, a central nitrate sensor. Nitrate deficiency, but not ammonium deficiency, abolishes Fe deficiency-induced chlorosis and suppresses the expression of Fe uptake genes (IRT1, FIT), confirming nitrate's specific signaling role. We show that Fe deficiency triggers rapid nuclear accumulation of NLP7 in a strictly nitrate-dependent manner. Loss-of-function nlp7 mutants exhibit attenuated Fe deficiency responses, including reduced FCR activity and diminished induction of IRT1, FRO2, and FIT, yet exhibit reduced chlorosis under Fe deficiency, indicating alleviation of stress symptoms rather than genuine enhancement of Fe tolerance. Transcriptome and molecular analyses identify NIGT1.3 as a direct transcriptional target of NLP7; NIGT1.3 in turn represses NRT1.1 transcription, establishing a regulatory cascade from nitrate sensing to Fe homeostasis modulation. Notably, growth-chlorophyll correlation analysis reveals that plant growth positively correlates with chlorophyll content under Fe sufficiency but negatively correlates under Fe deficiency, uncovering a growth-stress trade-off mediated by the NLP7-NIGT1.3 module. Collectively, our findings establish NLP7 as a central hub integrating nitrate signaling with Fe deficiency responses and reveal a regulatory mechanism that balances stress adaptation with growth maintenance under combined nitrate and Fe nutritional stress.

Soil salinization is increasingly threatening global agricultural productivity and food security, currently affecting over 6% of the world’s land and one-third of irrigated areas. Tomato (Solanum lycopersicum L.), a major vegetable crop worldwide, exhibits moderate sensitivity to salinity, which limits both its yield and fruit quality. In recent years, epigenetic regulation has gained attention as a key mechanism enabling flexible and reversible control of gene expression without altering DNA sequences. This review synthesizes current knowledge on the epigenetic control of salt stress responses in tomato, focusing on three interconnected levels: DNA methylation dynamics, RNA-directed DNA methylation (RdDM), and histone modifications. We explore how DNA methyltransferases reshape the methylome under salinity, using examples such as PKE1 and SlGI to illustrate functional gene-body methylation. The RdDM pathway is discussed with emphasis on the unexpected role of SlAGO4A as a negative modulator of stress tolerance and the growing evidence for RdDM-mediated regulation of transcription factors. We also examine the balanced regulation of histone acetylation and deacetylation, highlighting the conserved role of GCN5 in maintaining cell wall integrity and the diverse functions of HDACs (SlHDA1, SlHDA3, SlHDA5) in stress adaptation. Additionally, insights from wild tomato species and grafting-induced epigenetic changes are presented, revealing new dimensions of stress memory. Collectively, these epigenetic mechanisms constitute a complex regulatory framework that integrates stress responses with growth and development, providing potential targets for epigenetic breeding of salt-tolerant tomatoes.

Phosphate (Pi) deficiency dramatically reshapes root system architecture (RSA) in a species-dependent manner. In Arabidopsis thaliana, a well-studied STOP1-ALMT1 malate-exudation module promotes iron (Fe)-dependent reactive oxygen species (ROS) accumulation in root apices, leading to primary root (PR) inhibition. In contrast, agronomically important crops such as tomato (Solanum lycopersicum) exhibit PR promotion under Pi deficiency, but the underlying mechanisms remain unclear. Here, we show that in tomato the C2H2-type transcription factor SlSTOP1 promotes PR elongation under low Pi by activating citrate-dependent control of apoplastic iron (Fe) redox chemistry. Using Slstop1 and Slfrdl1 loss-of-function mutants, genomic complementation lines, and root co-culture assays, we demonstrate that SlSTOP1 induces the citrate transporter SlFRDL1 to drive citrate exudation, limiting Fe overaccumulation and spatially confined reactive oxygen species (ROS) accumulation in the root apex. Under Pi deficiency, disruption of SlSTOP1 or SlFRDL1 suppresses PR growth, enhances Perls/DAB-detected apoplastic Fe accumulation, and increases DAB/NBT-detected H₂O₂ and O₂·^- accumulation sites, whereas exogenous citrate or antioxidant treatment partially restores root growth. In vitro ferrozine and electron paramagnetic resonance assays further reveal that Fe-citrate complexes generate moderate Fe²⁺ and hydroxyl radicals compared with Fe-malate complexes, while low external H₂O₂ concentrations promote, but high concentrations inhibit, PR elongation. Together, these results identify a rewired SlSTOP1-SlFRDL1-citrate module that replaces the Arabidopsis STOP1-ALMT1-malate pathway, converting an inhibitory Fe-ROS signal into a growth-permissive redox regime and providing a mechanistic basis for species-specific root adaptation to Pi deficiency.

Nitrogen is a necessary macronutrient that limits plant growth and crop productivity, yet excessive fertilizer application has resulted in serious environmental consequences. The NIN-like protein (NLP) family consists of plant-specific transcription factors that serve as central regulators of nitrate signaling. In 2022, the discovery of NLP7 as an intracellular nitrate receptor represented a major conceptual shift from transcriptional regulation to signal perception. This review systematically summarizes the molecular architecture of NLP proteins, focusing on the conserved RWP-RK DNA-binding domain, the PB1 protein-protein interaction module, and the GAF-like domain associated with the integration of multiple signals. It also examines the species-specific expansion and evolutionary diversification of the NLP family, as well as the multilayered mechanisms that regulate NLP activity, including phosphorylation as a signal-dependent molecular switch, SUMOylation as a negative feedback mechanism, transcriptional regulation of downstream targets, and PB1-mediated protein interaction networks. In addition to nitrate signaling, NLPs serve as central hubs linking nitrogen and carbon metabolism and mediating responses to abiotic stresses including cold, heat, salinity, and iron deficiency. Notably, the NLP7–NIGT1.3 module coordinates a growth–stress trade-off during iron deficiency by modulating nitrate signaling intensity, revealing a previously unrecognized mechanism for balancing stress adaptation with growth maintenance. NLPs also participate in developmental processes, including lateral root formation and symbiotic nodulation. Finally, this review highlights the potential of NLP-based approaches for crop genetic improvement, such as overexpression of key NLP genes or CRISPR/Cas-mediated editing, to improve nitrogen use efficiency, stress tolerance, and yield. Collectively, these insights provide a theoretical foundation for developing crop varieties with improved nitrogen-use efficiency and context-dependent stress adaptation, while acknowledging the inherent trade-offs between productivity and resilience.