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Asparagine synthetase B (AS-B) is essential for nitrogen metabolism, but its broader physiological functions remain poorly understood. Here we show that the evolutionarily conserved Nicotiana benthamiana NbAS-B confers expression-dependent antiviral resistance and promotes plant growth. Multi-omics analyses indicate that NbAS-B-mediated antiviral immunity relies on glutamate-induced activation of Ca²⁺ signaling through the receptor GLR3.3, whereas its growth-promoting effect results from photosynthetic reprogramming. Building on these insights, we develop polyglutamate-loaded chitosan nanogels (PGANPs) to artificially manipulate this pathway. These nanogels efficiently enter plant tissues and enable sustained in situ release of glutamate, thereby mimicking and amplifying NbAS-B signaling outputs. PGANPs provide long-lasting systemic antiviral immunity while concurrently enhancing plant growth, without incurring metabolic costs. Our work identifies NbAS-B as a dual-function regulator linking metabolic status to immune activation and establishes PGANPs as an eco-friendly, controllable, and durable nanobiotechnology for managing viral diseases in crops. Controlling plant metabolism to improve growth and disease resistance has huge potential. Here, the authors find a conserved pathway which promotes antiviral resistance and promotes plant growth and develop polyglutamate-loaded chitosan nanogels to manipulate this pathway.

Identifying new molecular targets for novel anticancer treatments is a major challenge in clinical cancer research. We have shown that cytidine deaminase (CDA) expression is downregulated in about 60% of cancer cells and tissues. In this study, we aimed to develop a new anticancer treatment specifically inhibiting the growth of CDA-deficient tumor cells. High-throughput screening of a chemical library led to the identification of a naphthol derivative, X55, targeting CDA-deficient tumor cells preferentially, without affecting the growth of non-tumoral cells regardless of CDA expression status. Metabolomic profiling revealed that CDA-deficient HeLa cells differed markedly from control HeLa cells. X55 treatment had a moderate effect on control cells, but greatly disturbed the metabolome of CDA-deficient HeLa cells, worsening the deregulation of many metabolites. In particular, the levels of the three oncometabolites, fumarate, succinate and 2-hydroxyglutarate, were significantly lower in CDA-depleted cells, and this decrease in levels was exacerbated by X55 treatment, revealing an unexpected link between CDA deficiency, mitochondrial function and X55 response. Finally, we identified strong downregulation of MAPT (encoding Tau, a microtubule associated protein) expression as a reliable predictive marker for tumor cell X55 sensitivity.