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Rice serves as the staple food for over half of the world's population, yet its propensity to accumulate cadmium (Cd), a toxic heavy metal and potential human carcinogen, poses significant food safety concerns. OsNRAMP5, the primary transporter responsible for Cd and manganese (Mn) uptake in rice, has emerged as a key target for developing low-Cd rice varieties through breeding programs. However, the broader physiological roles of OsNRAMP5 beyond metal transport remain poorly understood. Here, we demonstrate that OsNRAMP5 mutations, while effectively reducing Cd accumulation, significantly compromise rice blast resistance by disrupting Mn homeostasis. Our mechanistic analysis reveals that Mn deficiency in osnramp5 mutants leads to reduced activities of critical defense enzymes, including manganese-dependent superoxide dismutase (Mn-SOD) and phenylalanine ammonia-lyase (PAL), resulting in decreased accumulation of hydrogen peroxide (H₂O₂) and lignin, which are essential components of plant defense responses. Furthermore, pathogen-induced expression of pathogenesis-related (PR) genes is markedly suppressed in osnramp5 mutants, indicating impaired immune signaling pathways. Importantly, our study also demonstrated that utilizing rice variety carrying major blast-resistance genes as a background can effectively eliminate the reduced rice blast resistance caused by OsNRAMP5 mutation. This study reveals an important trade-off between cadmium safety and disease resistance in rice breeding and provides a promising approach for developing rice varieties that balance low Cd accumulation with maintained blast resistance, informing breeding strategies that reconcile food safety and agronomic performance.
Zhou et al. (Mon,) studied this question.