Plant disease control is trapped in a constant evolutionary competition between plants and pathogens. Pathogens evolve

faster than we can breed resistance genes or register new fungicides. Notably, plants employ multiple immune strategies, including both disease resistance and tolerance, to protect their health, enriching the contextual understanding of plant defense mechanisms. Transgenic crops, while powerful, continue to face regulatory and public acceptance challenges in many regions, with

regulatory timelines varying across global frameworks. Meanwhile, chemical control faces an accelerating loss of efficacy due to resistance and is increasingly incompatible with climate-smart and biodiversity-friendly farming mandates. We argue that it is time to decouple crop immunity from plant genetics altogether and outsource it to an editable, transient, and regulation-resilient microbial layer: the endophyte microbiome.

Disruption of organelle interactions due to metabolic stress is a crucial factor in the pathological processes of many degenerative diseases. Compared with animal cells, the participation of chloroplasts enables plant cells to show defensive adaptation under stress. Therefore, delivering plant-derived photosynthetic systems into animal cells may help to establish a more stable organelle interaction network. Here, we show that plant-derived photosynthetic systems can effectively restore homeostasis of the interaction network of animal organelles. Specifically, plant-derived nanothylakoid units provide energy to animal cells, regulate intracellular Ca2+ homeostasis, increase endoplasmic reticulum (ER) lipid unsaturation and global membrane fluidity, reduce abnormal contact between mitochondria and ER, and alleviate mitochondrial dysfunction. By combining implantable light-emitting diodes with wireless charging, we expand photosynthesis therapy, enabling treatments for deeper tissues. This study provides a proof-of-concept for disease treatment based on the regulation of organelle interaction networks by natural photosynthetic systems and establishes a therapeutic approach for treating deep tissues. Unlike animals, plant possess mitochondria and chloroplasts and exhibit a unique defensive adaptation to stress. Here, the authors demonstrate the feasibility of restoring organelle interaction network homeostasis in animal cells by introducing plant-derived photosynthetic systems.

CRISPR‒Cas systems represent powerful tools for genome regulation. However, the large size of Cas proteins limits their efficient delivery via an adeno-associated virus (AAV), thereby restricting their clinical translation. Here, we engineer the IS200/IS605 transposon-encoded nuclease TnpB, along with its ωRNA scaffold, to create an enhanced TnpB system, which serves as a compact toolkit for gene activation, genome editing, and base editing. The gene activator enTnpBa increases expression by 2889-fold with a minimized 93 nt ωRNA and robustly activates endogenous genes in mammalian cells. We develop a single-AAV-based regimen for immune activation (AAV-ImmunAct) that delivers enTnpBa to activate CXCL9, IL-15, and IFN-γ. AAV-ImmunAct effectively enhances T cell migration and activation, increases killing of cancer cell lines and patient-derived organoids, and synergizes with anti-PD-1 therapy in humanized mice. Here, we establish enTnpB as a compact and versatile platform for genome regulation and a promising tool for cancer immunotherapy. CRISPR–Cas tools enable genome regulation but are often too large for efficient AAV delivery. Here, authors engineer a compact enhanced TnpB–ωRNA system (enTnpB) as a versatile genome regulation platform and develop a single-AAV regimen, ImmunAct, to activate endogenous cytokines and enhance cancer immunotherapy.

Rapid identification of viral infections and specific variants in patient samples requires a simple and multiplexed RNA detection method that does not rely on DNA sequencing. Although recent direct detection assays based on CRISPR–Cas13a offer rapid RNA detection by avoiding reverse transcription and DNA amplification required of gold-standard PCR assays, these assays are not easily multiplexed to detect multiple viruses or variants without dividing the sample into separate reactions. Here we show that Cas13a acting on single-target RNAs exhibits variable nuclease activity that depends on the interaction between the target RNA and crRNA. To exploit this feature for multiplexed detection, we devised a crRNA modification strategy that enables programmable tuning of Cas13a’s nuclease enzymatic rates. Using a droplet-based Cas13a assay, we demonstrate that kinetic signatures can be harnessed to differentiate among respiratory viruses and SARS-CoV-2 variants in contrived and clinical samples. This kinetic barcoding strategy can be extended to additional RNA targets through simple modification of crRNAs. A multiplexed RNA detection method exploits crRNA-dependent variability in Cas13a activity on RNA targets for kinetic barcoding and can be used to distinguish among SARS-CoV-2 variants in clinical samples.

Although considerable research has been conducted on how bacteria respond to temperature, there are still few studies that use simple protein allocation models to characterize these responses. To bridge this gap, we utilize a protein allocation framework to delineate quantitative correlations among temperature, growth rate, and the fraction of functional protein sectors. By calibrating the model with experimental temperature-dependent growth curves of Escherichia coli, we predict how proteomic resources are reallocated across various temperatures. This approach enables us to elucidate, from a proteomic perspective, the temperature dependency of constitutive β-galactosidase expression and the variations in E. coli cell size. Our research deepens the understanding of bacterial physiological adaptation to temperature changes.

Protein malnutrition remains a major global health challenge, particularly in regions where cereal grains dominate daily diets and access to diverse protein sources is limited. Cereals such as rice, wheat and maize provide most of the world’s calories, yet their grain proteins are often low in essential amino acids and poorly balanced for human nutrition. Improving both the quantity and quality of cereal protein therefore represents a critical opportunity to enhance human health while reducing reliance on environmentally intensive animal-based foods. In this Review, we synthesize recent advances in understanding how grain protein content and composition are regulated in cereals, and why protein enhancement has historically been constrained by trade-offs with starch accumulation and yield. We discuss how domestication and modern breeding reshaped carbon and nitrogen allocation in cereal grains, creating a starch-dominant optimum that limits protein concentration. Drawing on genetic studies from rice, maize and wheat, we highlight emerging strategies that improve nitrogen acquisition, amino acid transport, storage protein composition and endosperm buffering capacity, enabling partial decoupling of protein accumulation from yield penalties. Finally, we place cereal protein biofortification within a broader nutritional and environmental context. Enhancing protein density and amino acid balance in staple cereals can improve dietary adequacy for vulnerable populations while lowering greenhouse gas emissions per unit of nutrition. Together, these insights position cereal protein biofortification as a scalable and equitable pathway towards healthier diets and more sustainable food systems under global climate and population pressures. Cereal protein biofortification can improve nutrition while maintaining yield and lowering environmental impact. This Review shows how genetics and breeding can enhance protein quality in staple cereals to support healthier and more sustainable diets.