Overall, this review highlights the potential importance of nutrient homeostasis, redox regulation, and susceptibility modulation as components of future research aimed at developing climate-resilient and nutritionally improved wheat cultivars.
Abstract
The increasing threat posed by wheat rust diseases caused by Puccinia spp. necessitates the development of resistance strategies that extend beyond conventional race-specific mechanisms. Although recent reviews (2023–2025) have emphasized gene discovery and genomic approaches, comparatively less attention has been given to the potential roles of metabolic regulation and micronutrient homeostasis in host–pathogen interactions. Here, we present a narrative synthesis of current evidence and propose a conceptual framework in which induced mutagenesis (ethyl methanesulfonate, EMS, and γ-irradiation) serves as a tool for investigating interactions among redox regulation, iron (Fe) homeostasis, and disease resistance. A key component of this framework is the proposed interplay between reactive oxygen species (ROS) signaling and Fe partitioning. Vacuolar iron transporters (VITs), ferritins, and associated transport networks regulate intracellular Fe distribution and may influence Fe availability at the host–pathogen interface, potentially affecting fungal development and host defense responses. This concept of “iron-withholding immunity” may operate alongside ROS-mediated defense processes, linking metabolism with immune function. Observations from mutant wheat populations are broadly consistent with the hypothesis that these processes may contribute to durable adult-plant resistance (APR), which is characterized by reduced disease development, coordinated defense responses, and relative stability across environments. In some studies, Fe-enriched mutant lines have been associated with enhanced expression of pathogenesis-related genes and the occurrence of combined APR and seedling-resistance phenotypes, suggesting possible links between micronutrient homeostasis and immunity. Integration of high-throughput phenotyping with genotype × environment × time (G × E × T) frameworks may further improve our understanding of quantitative resistance and disease-associated traits. Overall, this review highlights the potential importance of nutrient homeostasis, redox regulation, and susceptibility modulation as components of future research aimed at developing climate-resilient and nutritionally improved wheat cultivars.
Atmospheric CO₂ concentration is projected to rise substantially over the coming decades, yet its impact on the molecular mechanisms governing plant immunity remains poorly understood. Here, we investigated how elevated CO₂ (eCO₂; 650 ppm) combined with increased temperature (+5 °C) influences tomato responses to Botrytis cinerea through integrated phenotypic, metabolomic, transcriptomic, and gene regulatory network (GRN) analyses across eight cultivars. Although cultivars displayed contrasting susceptibility under ambient conditions, eCO₂ consistently enhanced tolerance across all genetic backgrounds. Multi-omics analyses revealed a partial uncoupling between transcriptional and metabolic responses during infection, with repression of photosynthesis- and carbon metabolism- related genes contrasting with the accumulation of carbon- and amino acid-derived metabolites. Under eCO₂, this metabolic disruption was attenuated, preserving metabolic homeostasis during infection. GRN reconstruction identified a conserved WRKY–ERF regulatory module underlying the growth–defence trade-off, while functional perturbation demonstrated that its contribution to resistance depends on both genotype and environmental context, highlighting the importance of basal defence mechanisms. Targeted metabolomics further revealed that eCO₂ promotes a metabolically primed state characterized by reinforcement of structural and chemical defence barriers rather than stronger activation of inducible immune responses. Together, our findings show that enhanced tolerance under eCO₂ emerges from coordinated reorganization across regulatory and metabolic networks, providing a systems- level framework for understanding plant immunity and improving crop resilience under future climate scenarios.
Francesca Baistrocchi, Marta Orero-Bayo, Lili Yu et al.· bioRxiv· 0 citations
Molecular insights of host–pathogen interactions offer decoding of sustainable strategies for developing resilient cultivars and effective management of false smut disease, highlighting stage-specific pathogenicity genes and rice defense mechanisms that control false smut disease development.
P. Parmar, B. Bashyal· Plant Molecular Biology· 0 citations
Current knowledge of the molecular mechanisms underlying wheat-Pst interactions are synthesized, key advances in understanding their reciprocal communication are highlighted, and emerging directions for developing durable resistance are discussed.
Jicheng Qu, Fengchang Ye, Baishan Liu et al.· Physiologia Plantarum : An I...· 0 citations
A temporally ordered, multi-layered defense network in B. napus is revealed, characterized by sequential metabolic reprogramming, immune signaling activation, and structural reinforcement, providing mechanistic insights into L. biglobosa resistance.
Yong-Yi Xia, Haiyan Huangfu, Mengjiao Yan et al.· Frontiers in Plant Science· 0 citations
Nonhost resistance (NHR) provides durable and broad-spectrum protection against non-adapted pathogens, yet its regulatory mechanisms in crops remain poorly understood. Here, we show that salicylic acid (SA) signaling plays a critical role in potato NHR against the oomycete pathogen Phytophthora capsici. SA-deficient NahG transgenic plants developed spreading water-soaked lesions following inoculation, whereas wild-type plants exhibited only localized necrosis. Exogenous SA treatment partially restored resistance in NahG lines, supporting an important role for SA in potato NHR. Transcriptome analysis revealed that SA deficiency suppressed defense-associated pathways, including MAPK signaling and pathogenesis-related (PR) gene expression, while inducing photosynthesis- and carbohydrate metabolism-associated genes. In addition, transcriptomic data suggested altered hormone-associated signaling, including induction of ABA-, IAA-, and JA-related pathways, indicating broad transcriptional changes in response to SA deficiency. Functional assays further demonstrated that silencing ERF1B enhanced susceptibility, whereas silencing WRKY53 increased resistance, suggesting distinct transcriptional regulatory roles downstream of SA signaling. Together, these findings support a central role for SA in coordinating immune signaling and metabolic responses during potato nonhost resistance. This study provides new insights into the regulatory framework underlying potato-oomycete interactions.