RpfF is a bifunctional enzyme. Using a single active site, it performs two chemically distinct reactions. As an enoyl-acyl carrier protein (ACP) dehydratase, it helps convert intermediates of the bacterial fatty acid synthesis pathway, known as FASII, into the DSF family of signaling molecules, which include DSF, BDSF, IDSF, and CDSF. As an acyl-ACP thioesterase, it cleaves the thioester bond linking fatty acid chains to ACP, releasing free fatty acids. While the dehydratase role in quorum sensing has been studied extensively, the physiological purpose of the thioesterase activity remained a puzzle for more than a decade.

The clue that something more was going on came from earlier work showing that deleting the rpfF gene from Xoo caused a striking loss of membrane integrity. The mutant became hypersensitive to detergents, leaked proteins, and lost much of its ability to cause disease. But because rpfF deletion removes both enzymatic activities at once, it was unclear which function was responsible. The research team, led by Lizhen Luo, Zhe Hu, and Haihong Wang of South China Agricultural University together with John E. Cronan of the University of Illinois, resolved this ambiguity with an elegant trick: they replaced the missing thioesterase activity with unrelated enzymes borrowed from other organisms.

The team inserted into the chromosome of the rpfF deletion mutant two foreign thioesterase genes: tesA from the gut bacterium Escherichia coli and fatB1 from the camphor tree, Cinnamomum camphorum. Because these enzymes share no evolutionary history with RpfF and cannot make DSF signals, any rescue of the mutant’s defects could be attributed squarely to thioesterase chemistry. The results were unambiguous. Both foreign enzymes restored the mutant’s resistance to the detergents sodium dodecyl sulfate and Triton X-100, its tolerance of osmotic and oxidative stress, and its normal low permeability to fluorescent dyes. Adding purified DSF signal to the mutant, by contrast, did nothing for detergent sensitivity, proving that the membrane protection comes from thioesterase activity itself rather than from quorum sensing.

Microscopy drove the point home visually. Under scanning electron microscopy, untreated cells of the mutant looked normal, but exposure to detergent caused the rpfF deletion strain to undergo extensive lysis, spilling its intracellular contents, while wild-type cells and thioesterase-complemented strains remained largely intact. Transmission electron microscopy showed cytoplasmic aggregation and loss of electron density in the mutant under detergent stress, changes that were markedly milder in the complemented strains. Consistent with a repaired membrane, the mutant’s abnormal leakage of extracellular proteins, including cellulase, xylanase, and lipase, fell back toward wild-type levels when any of the three thioesterases was expressed, and an engineered green fluorescent protein that had escaped from the mutant’s cells was once again retained inside.

The lipid analysis explained why. In Gram-negative bacteria, membrane integrity depends on a delicate stoichiometric balance between phospholipids and lipopolysaccharide (LPS), as well as on the precise mix of fatty acyl chains within those lipids. Pulse-labeling experiments with radioactive acetate showed that the rpfF mutant accumulated excess phospholipids, particularly phosphatidylethanolamine and cardiolipin, while its LPS content dropped sharply: the lipid A-to-phospholipid ratio fell from 0.117 in the wild type to 0.037 in the mutant. Gas chromatography-mass spectrometry further revealed a skewed fatty acid profile, with the unsaturated C16:1 species rising and the saturated C16:0 and branched iso-C17:0 species falling. Expression of rpfF, tesA, or fatB1 corrected both the phospholipid-to-LPS ratio and the fatty acid composition.

The deepest defect turned out to be in the rate of fatty acid synthesis itself. Radiolabel incorporation showed that the rpfF mutant manufactured fatty acids at only about one-third of the wild-type rate, and specific synthesis rates measured by scintillation counting confirmed the slowdown. Complementation with any of the thioesterase genes restored synthetic flux to near-wild-type levels. The authors propose that when RpfF is absent, medium-chain acyl-ACPs accumulate inside the cell and feed back to inhibit the FASII machinery, throttling the supply of fatty acids needed to build phospholipids and LPS. By hydrolyzing excess acyl-ACPs, the thioesterase relieves this feedback inhibition and keeps membrane biogenesis running.

Crucially, the thioesterase also rescued virulence. In leaf-clipping assays on susceptible rice plants, the wild-type strain produced lesions averaging 17.8 centimeters at fourteen days after inoculation, while the rpfF mutant produced lesions of only 2.1 centimeters, an 88 percent reduction. Expressing the E. coli or plant thioesterase restored lesion lengths to 12.5 and 10.1 centimeters respectively, approaching the 13.3 centimeters achieved by restoring the native rpfF gene. Bacterial counts within lesions were only marginally lower in the mutant, indicating that the virulence defect reflects failed tissue colonization rather than poor growth inside the plant. Notably, exopolysaccharide production, which collapsed fourfold in the mutant, was restored only by native rpfF and by DSF signaling, not by the foreign thioesterases, showing that EPS is governed by quorum sensing while most other virulence traits ride on membrane health.

The study also showed that the thioesterase function is conserved across the genus and is itself wired into quorum sensing. Deleting rpfF in the related pathogen Xanthomonas campestris pv. campestris likewise caused detergent sensitivity and a skewed phospholipid-to-LPS ratio, and a foreign thioesterase repaired the damage. Moreover, overproducing the sensor kinase RpfC in wild-type Xoo mimicked the mutant’s detergent hypersensitivity, and the isolated receiver domain of RpfC inhibited purified RpfF’s thioesterase activity in vitro, extending to Xoo the known mechanism by which RpfC physically blocks RpfF in X. campestris. The authors propose a dual-function model in which RpfF simultaneously maintains lipid homeostasis through its thioesterase activity and produces DSF signals through its dehydratase activity. As cell density rises and DSF accumulates, RpfC’s grip on RpfF loosens, accelerating fatty acid synthesis and remodeling the membrane to withstand host-imposed stresses. In this way, the pathogen synchronizes virulence factor production with adaptive membrane restructuring, and the divergent phenotypes long observed between rpfF mutants of different Xanthomonas species are reinterpreted as the interplay of a conserved membrane-maintenance function with species-specific quorum-sensing circuitry. The work opens a potential avenue for anti-virulence strategies: disrupting RpfF’s thioesterase activity could strip the pathogen of both its signals and its structural resilience at once.

Subject of Research: The dual dehydratase and thioesterase activities of the RpfF enzyme in Xanthomonas oryzae pv. oryzae and their roles in fatty acid synthesis, membrane integrity, and virulence

Article Title: The RpfF Acyl-ACP thioesterase of major rice pathogen Xanthomonas oryzae pv . oryzae is essential for maintenance of membrane function and virulence

Article References: Luo, L., Hu, Z., Yan, M., Cronan, J. E., & Wang, H. (2026). The RpfF Acyl-ACP thioesterase of major rice pathogen Xanthomonas oryzae pv. oryzae is essential for maintenance of membrane function and virulence. PLOS Pathogens, 22(10), e1014669. https://doi.org/10.1371/journal.ppat.1014669

Image Credits: AI Generated

DOI: 10.1371/journal.ppat.1014669

Keywords: Xanthomonas oryzae, RpfF, thioesterase, fatty acid synthesis, membrane integrity, quorum sensing, DSF, virulence, rice bacterial leaf blight, phospholipids, lipopolysaccharide, RpfC

The research, led by Shivranjani Baruah of Cornell University together with collaborators at Cornell, the International Crops Research Institute for the Semi-Arid Tropics (ICRISAT) in Hyderabad, and the Indian Institute of Rice Research, set out to answer a deceptively simple question: can a four-band multispectral sensor paired with 3D laser scanning classify bacterial blight severity as reliably as the expensive hyperspectral systems that dominate the field? The answer, in most cases, is yes — provided the data are processed in the right way.

The team conducted their experiments on the LeasyScan platform at ICRISAT, an outdoor high-throughput phenotyping facility that moves plants past a Phenospex sensor combining LiDAR-based 3D reconstruction with RGB and near-infrared imaging. Ten rice genotypes were crossed with four Xoo bacterial strains, producing 17 unique host-pathogen combinations that spanned the full spectrum of disease outcomes, from complete resistance to extreme susceptibility. The panel included near-isogenic IRBB lines each carrying a single known resistance gene — executor genes, NLR proteins, receptor-like kinases, and recessive alleles of susceptibility genes — alongside four popular southern Indian cultivars that serve as susceptible checks. After clip inoculation, plants were scanned daily from the day of inoculation until 16 days post inoculation, while two independent plant pathologists scored disease severity on the standard six-point scale derived from the International Rice Research Institute’s Standard Evaluation System.

The resulting dataset of 3,073 3D point clouds became the raw material for a series of machine learning experiments. The key insight came from how the spectral data were handled. Conventional approaches typically average vegetation indices — mathematical combinations of reflectance values that track chlorophyll content, pigment degradation, and senescence — across an entire plant canopy. But bacterial blight does not attack a canopy uniformly. It begins as water-soaked lesions that expand into necrotic patches, leaving healthy and diseased tissue intermingled on the same leaves. Averaging, the researchers reasoned, throws away exactly the information that matters most.

To test this, the team developed two complementary ways of preserving within-canopy spectral heterogeneity. The first was supervised binning: for each vegetation index, five thresholds were optimized using simulated annealing to divide continuous index values into six bins, with the objective of maximizing the separation between disease severity classes. Each point cloud was then summarized by the proportion of points falling into each bin. The second was unsupervised: k-means++ clustering with 12 clusters partitioned point-level spectral features into recurrent spectral states, and each plant was described by the relative abundance of each state within its canopy. Kernel density estimation confirmed that vegetation indices such as NDVI, SRI, and PSRI shifted systematically with severity — NDVI, for example, declined from 0.558 in healthy plants to 0.500 in highly susceptible ones — and Kolmogorov-Smirnov tests showed significant differences among all severity classes for every index examined.

The results were striking. When severity was classified into four broad categories — healthy, moderately resistant, susceptible, and highly susceptible — a random forest model trained on binned vegetation indices alone achieved 76.2 percent accuracy on an independent holdout test set, with a weighted F1 score of 0.76 and a quadratic weighted kappa of 0.86, a measure that penalizes large misclassifications more heavily than small ones. The mean absolute error was just 0.28 class units. Adding cluster-ratio features or structural traits from the 3D scans did not meaningfully improve on this. By contrast, models built on conventional canopy-average vegetation indices lagged behind, reaching only 69.7 percent accuracy. The gap widened when the task was made harder: for the original six-category scale, the best average-index model managed just 58 percent accuracy, while a support vector machine combining cluster ratios and binned indices reached 71 percent.

The pattern held across algorithms. XGBoost performed poorly in every configuration, while random forest and support vector machines traded the lead depending on the classification task. Feature importance analysis revealed that binned indices such as NGBI, HUE, PSRI, GRVI, and VARI dominated the top predictors, alongside a handful of cluster-ratio variables. Notably, the models were never told which genotype, bacterial strain, or day post inoculation each scan came from — they had to infer severity purely from the spectral and structural signatures of the plants themselves. Error analysis showed that misclassifications clustered in specific genotypes, particularly the resistant lines IR10, IR21, and IR5, and were concentrated between neighboring severity classes, suggesting that adjacent categories form a biological continuum rather than sharply separable states.

That finding has practical implications for breeding programs. If fine distinctions between neighboring severity scores are inherently unstable — influenced by lesion distribution, symptom timing, lighting, canopy architecture, and scorer subjectivity — then selection decisions may benefit more from robustly separating broad resistance classes than from chasing unreliable precision on a fine scale. The four-class framework delivered exactly that: reliable discrimination between healthy, intermediate, and susceptible responses, with the healthiest class classified with 93 percent recall and the most susceptible at 78 percent.

What makes the study genuinely exciting is its economics. Hyperspectral imaging systems, which measure reflectance across dozens or hundreds of narrow wavelength bands, can cost prohibitive amounts and demand serious computational resources — barriers that put them out of reach for many breeding programs in the very regions where rice disease pressure is highest. This work demonstrates that a simple four-band sensor, the kind already mounted on consumer drones and agricultural scanners, can deliver usable classification accuracy if paired with 3D structural context and heterogeneity-preserving data processing. The 3D component matters because it lets researchers interpret spectral signals in their spatial context within the canopy, capturing subtle changes in leaf angle and leaf area that flat imaging misses.

The authors are careful to note the limitations. Severity labels themselves carry uncertainty, especially for intermediate classes where visual assessment is subjective. The models do not yet exploit explicit lesion localization or temporal progression, and some degree of confounding between disease severity and plant developmental stage is possible. Broader validation across seasons, environments, and genetic backgrounds will be needed before the framework becomes a routine breeding tool. The team has made its models, processed datasets, and analysis pipelines publicly available to accelerate that process. But the direction of travel is clear: as laser and depth sensors become cheaper and more portable, the combination of low-dimensional spectral sensing with 3D phenomics could bring objective, high-throughput disease screening within reach of the breeding programs that need it most — and not just for rice. The framework could be adapted for foliar diseases across many crops, potentially accelerating resistance breeding at a moment when food security under climate stress has never mattered more.

Subject of Research: 3D multispectral phenotyping for rice bacterial blight severity classification

Article Title: A practical framework for rice bacterial blight severity classification using 3D multispectral sensing

Article References: Baruah, S., Du, R., Kumar, D., Laha, G., Choudhary, S., Kholova, J., Jiang, Y., Bogdanove, A. J., & Gold, K. M. (2026). A practical framework for rice bacterial blight severity classification using 3D multispectral sensing. Smart Agricultural Technology, 15, Article 102586. https://doi.org/10.1016/j.atech.2026.102586

Image Credits: AI Generated

DOI: 10.1016/j.atech.2026.102586

Keywords: rice, bacterial blight, Xanthomonas oryzae, 3D phenotyping, multispectral imaging, machine learning, vegetation indices, plant breeding, disease severity, LiDAR, food security, precision agriculture

The technology at the heart of the study is called MHISR, short for microscopic hyperspectral image super-resolution. Hyperspectral imaging captures hundreds of narrow wavelength bands for every pixel, revealing chemical and structural information invisible to ordinary cameras. It has become a powerful non-destructive method for monitoring plant health, but conventional systems operate at millimeter-level resolution, restricting most disease monitoring to the canopy or whole-leaf scale. Microscopic hyperspectral imaging pushes the technique down to the micro-scale, but hardware limitations take a heavy toll: spatial resolution drops and spectral signals become contaminated with noise and mixing, leaving critical microscopic features buried in background interference. The research team, led by Ping Sun and Xuping Feng, set out to solve this problem computationally rather than by rebuilding expensive optics.

MHISR is a spatial-spectral fusion network built on an enhanced convolutional neural architecture, and its design reflects a careful analysis of what existing approaches cannot do. Convolutional neural networks excel at recovering spatial textures but, because of their limited local receptive fields, struggle to preserve long-range spectral correlations across hundreds of bands. Transformer-based models can capture global dependencies but demand enormous training data and computational resources. The promising Mamba architecture, based on selective state-space models, offers long-range modeling with linear complexity, yet conventional versions rely on one-dimensional sequential scanning that disrupts spatial relationships and loses detail. MHISR sidesteps these trade-offs with two parallel branches: a spatial branch that combines local convolutional feature extraction with a residual multi-dconv transposed attention mechanism to preserve fine stomatal edges, and a spectral branch built around a bidirectional Mamba module that scans forward and backward through the spectral sequence to model cross-band dependencies with linear complexity.

Within the spatial branch, a novel multi-path attention extraction module suppresses the complex high-frequency noise typical of microscopic imagery. It works through three complementary paths: a distillation path that compresses channels and strips away redundant background to isolate the geometric morphology of stomatal edges, a remain path that preserves spatial continuity in the untouched channels, and an enhance path that applies global pixel-wise correlation to amplify the subtle textural variations induced by disease. The spectral branch’s 3D spectral module couples local spatial-spectral convolutions with channel attention and then reshapes features into spectral sequences for the bidirectional state-space scan. An adaptive weighted fusion module then learns, pixel by pixel, how best to merge the two streams, while a global residual learning strategy accelerates convergence. The result is a network that jointly preserves local microstructural fidelity and global spectral continuity.

To train and test the system, the researchers built a microscopic hyperspectral dataset spanning four crops with very different leaf topologies and stomatal distributions: rice, maize, tomato, and chili pepper. A MicroHSIVNIR10H hyperspectral imaging system coupled to a metallurgical microscope acquired reflective images across 400 to 1000 nanometers with a spectral resolution of 5 nanometers or better, using push-broom scanning and a prism-grating-prism splitting unit. After Savitzky-Golay smoothing removed edge noise, 179 usable spectral bands remained, far exceeding common public hyperspectral datasets such as CAVE with 31 bands or Houston with 64. Sliding-window cropping produced 1336 patches of 256 by 256 pixels as ground truth, which were downsampled fourfold with bicubic interpolation to create the low-resolution inputs the network had to reconstruct.

The performance results were decisive. Benchmarked against six established super-resolution methods, including bicubic interpolation, GDRRN, MCNet, SSPSR, the transformer-based ESSAFormer, and the dual-domain SRDNet, MHISR achieved the best score on every one of six evaluation metrics. It reached a peak signal-to-noise ratio of 37.33 decibels, a full 1.15 decibels above the second-best method, and reduced the spectral angle mapper value from 1.142 to 1.096, an improvement of roughly 5.8 percent in spectral fidelity. Its correlation coefficient of 0.998 indicates near-perfect agreement with the ground truth. Remarkably, this accuracy came with modest computational cost: the network contains only about 2.09 million parameters and requires 1.227 teraflops, roughly ten times fewer than MCNet. Ablation experiments confirmed that the two branches are genuinely complementary, with removing either module degrading performance and the full model substantially outperforming either half alone.

The real payoff came when the team turned the sharpened images toward rice disease evaluation. They worked with the rice variety Haifeng-1 and resistant lines derived from it through gamma-ray irradiation mutagenesis, classified as highly resistant or low resistance based on their responses to Xanthomonas oryzae pv. oryzae. Flag leaves were inoculated with bacterial suspension using the standard leaf-clipping technique, and lesions appeared within seven days, confirming successful colonization. When the trained MHISR network reconstructed hyperspectral images of infected stomatal regions, clear spectral fingerprints emerged. Low-resistance leaves showed significantly higher reflectance at 470 nanometers, in the blue region governed by chlorophyll and carotenoid absorption, indicating that pathogen invasion had damaged chloroplast structure in guard cells and depleted pigment content. They also exhibited a blue shift of the red edge near 710 nanometers, a classic signature of stress-induced chlorophyll degradation, and reduced reflectance in the near-infrared beyond 750 nanometers, suggesting that severe infection compromised the internal cellular structures responsible for light scattering.

Texture analysis added a second layer of evidence. Using the gray-level co-occurrence matrix, the researchers found that entropy and contrast values were significantly higher in low-resistance stomatal regions, while correlation was significantly lower, indicating that the pathogen disrupts the regular cellular architecture of the stomatal complex and produces statistically measurable tissue heterogeneity. A support vector machine classifier trained on these features showed that fusing spectral and textural information from the super-resolution images outperformed every alternative, achieving an accuracy of 0.96 and an F1-score of 0.94, and even exceeding models built on the original high-resolution ground truth images. This finding carries a striking implication: the AI-reconstructed images contained texture details so faithful that they revealed microscopic phenotypic variation more effectively than the raw high-resolution data itself.

From the most informative variables, the team distilled a new quantitative metric, the stomatal disease resistance index, which combines the ratio of reflectance at 710 and 470 nanometers with the entropy texture feature. The spectral ratio captures pathogen-induced pigment degradation and red-edge structural changes, while entropy quantifies the spatial heterogeneity of guard-cell damage, so a higher index signals more severe stomatal impairment. Statistical analysis confirmed a highly significant difference in the index between the resistant and susceptible lines, positioning it as a sensitive digital biomarker for early-stage bacterial leaf blight stress. For breeders screening candidate varieties, such an index could translate the invisible physiology of stomatal defense into a single, comparable number, accelerating the development of disease-resistant rice.

The authors are careful to note the limits of the current work. Disease assessments so far rest on controlled inoculation experiments with relatively limited datasets, and the framework has yet to face the messier conditions of real fields, where lighting, humidity, and mixed infections complicate every measurement. Future work will expand the datasets and validate the approach across a broader range of crop-specific disease scenarios. Even so, the study marks a meaningful convergence of imaging physics, plant pathology, and machine learning. By teaching an algorithm to see the microscopic world more clearly than the hardware that captured it, the researchers have opened a path toward digital, early-stage plant phenotyping at the scale where plant immunity actually plays out, one stoma at a time.

Subject of Research: Deep learning-based super-resolution of microscopic hyperspectral images for evaluating rice bacterial leaf blight resistance at the stomatal level

Article Title: MHISR: A spatial-spectral fusion network for microscopic hyperspectral image super-resolution with application in rice disease evaluation

Article References: Sun, P., Du, M., Qi, M., Sun, C., Xia, Z., He, Y., Zhang, Z., & Feng, X. (2026). MHISR: A spatial-spectral fusion network for microscopic hyperspectral image super-resolution with application in rice disease evaluation. Artificial Intelligence in Agriculture. https://doi.org/10.1016/j.aiia.2026.08.018

Image Credits: AI Generated

DOI: 10.1016/j.aiia.2026.08.018

Keywords: hyperspectral imaging, super-resolution, deep learning, rice disease, bacterial leaf blight, stomata, Mamba architecture, plant pathology, disease resistance index, machine learning, agricultural imaging, Xanthomonas oryzae

The commentary centers on a study by Zhang and colleagues published in Molecular Plant, which examined how the gaseous signaling molecule hydrogen sulfide, or H2S, influences the balance between immunity and development in rice. Hydrogen sulfide has long been recognized as a versatile player in plant physiology. It promotes seed germination by activating antioxidant enzymes and MAPK signaling pathways, enhances photosynthetic efficiency by upregulating photosynthetic enzymes and light signaling responses, and suppresses chlorophyll degradation to delay senescence. Under abiotic stresses such as heavy metal contamination, drought, heat, cold, and salinity, H2S bolsters resilience through enhanced antioxidant activity, protection of the photosynthetic apparatus, regulation of sulfur metabolism, and crosstalk with phytohormones. It also participates in defense against pathogens and herbivores by inducing pathogenesis-related gene expression, modulating glutathione metabolism, and interacting with hormone signaling networks.

What has remained poorly understood, however, is how H2S fits into the growth-defense trade-off itself. The resource constraint hypothesis, one of the most prevalent explanations for this trade-off, holds that plants possess finite energy and materials, so any reallocation toward defense necessarily diminishes what is available for growth. Yet accumulating evidence suggests that plants do not simply passively divide a fixed budget. Instead, they actively regulate the balance through a sophisticated, multi-layered regulatory network in which hormone crosstalk plays a central role, supplemented by microRNAs and non-coding RNAs, epigenetic regulation, and post-translational modifications of key transcription factors and NLR immune receptors. The new work adds an unexpected layer to this network: a redox-controlled structural transition of a single metabolic enzyme.

Zhang and colleagues began with a simple observation: applying H2S externally to rice plants improved their resistance to two devastating bacterial pathogens, Xanthomonas oryzae pv. oryzicola and Xanthomonas oryzae pv. oryzae, the causal agents of bacterial leaf streak and bacterial blight respectively. The treatment triggered the release of hydrogen peroxide, a burst of reactive oxygen species, and the expression of defense genes. But there was a cost. The same treatment stunted root elongation and impaired the development of lateral roots, a textbook manifestation of the growth-defense trade-off. The question became how the plant could harness the defensive benefits of H2S while avoiding its developmental penalties.

The answer lay in a protein called OsCBSX3, a rice protein containing a cystathionine beta-synthase domain. CBS domain-containing proteins are homologs of enzymes known from mammals, where they catalyze the condensation of cysteine and homocysteine to form cystathionine and H2S. The researchers showed that OsCBSX3 positively regulates rice resistance to both Xoc and Xoo, and that this protective function depends on its ability to produce hydrogen sulfide. Crucially, like other CBS domain-containing proteins, OsCBSX3 exists in two distinct structural states within the plant: a monomeric form and an oligomeric form. When bacteria infect the plant, monomeric OsCBSX3 shifts into the oligomeric state, and this oligomer can enter the chloroplast, the energy-producing organelle of the cell.

The functional importance of this structural conversion was demonstrated through genetics. An oligomerization-deficient mutant of OsCBSX3 showed impaired H2S production, compromised resistance against Xanthomonas oryzae, and defective chloroplast localization. In other words, the ability of the protein to assemble into its multi-subunit form is not a structural curiosity but the very mechanism by which the plant ramps up sulfide-based signaling during an attack. The oligomeric state is the immune-active state, and the monomeric state is the quiet, growth-compatible state.

To understand how this toggle is itself controlled, the team searched for proteins that physically interact with OsCBSX3 and identified two partners: OsTrxZ, a member of the thioredoxin family of redox proteins, and OsPsbO, the manganese-stabilizing protein of photosystem II. The picture that emerged is elegantly self-regulating. Upon pathogen infection, PsbO binds to OsCBSX3 and promotes its monomer-to-oligomer transition, elevating H2S generation and thereby enhancing disease resistance. But once H2S levels rise too high, a second interaction takes over: TrxZ competes with PsbO for binding to OsCBSX3 and reduces the protein back to its monomeric form. This monomerization curtails further H2S synthesis, alleviating the overaccumulation of the gas and its detrimental impacts on growth and development. The system thus functions as a negative feedback loop, with the signal itself, H2S, triggering the shutdown of its own production.

The significance of this finding extends beyond rice pathology. As Pu and colleagues emphasize in their commentary, the study provides the first evidence that H2S plays a coordinating role in plant growth-defense trade-offs and reveals the underlying mechanism. It also overturns a long-standing assumption about how plants make hydrogen sulfide in the first place. Until now, H2S production in plants was attributed almost exclusively to cysteine desulfurization enzymes, namely L-cysteine desulfhydrase and D-cysteine desulfhydrase. The demonstration that a CBS domain protein catalyzes H2S synthesis in plants fills a genuine gap in the field and suggests that the enzymology of sulfide signaling is more diverse than previously appreciated. It also illustrates a universal strategy for managing the growth-defense trade-off: rather than changing gene expression wholesale, the plant dynamically tunes the metabolic activity of a single enzyme by switching its oligomeric state.

For breeders, the practical implications are considerable. OsCBSX3, PsbO, and OsTrxZ together constitute a module of potential targets for engineering disease resistance in rice, one of the world’s most important staple crops feeding billions of people. The commentary’s authors are careful to note, however, that the goal is not simply to maximize H2S production. Concentration thresholds must be optimized so that resistance is deployed on demand, avoiding the excessive growth inhibition that would erode any yield advantage gained from disease resistance. They point to precise gene editing techniques, including the use of pathogen-inducible promoters that would activate the defense module only when a threat is detected, as a plausible route to achieving this kind of calibrated immunity.

The work also reframes how scientists think about trade-offs in general. The resource constraint hypothesis remains valid as a broad principle, but the OsCBSX3 story shows that plants possess dedicated molecular machinery for actively arbitrating between growth and defense, rather than merely suffering the consequences of a fixed budget. A gaseous signal, a photosynthetic protein, a thioredoxin, and a metabolic enzyme form a self-correcting circuit that boosts immunity during infection and quietly stands down when the danger has passed or when the cost to the plant becomes too great. Understanding such circuits in rice may well presage similar discoveries in other crops, opening a path toward plants that no longer have to choose between thriving and surviving.

Subject of Research: Hydrogen sulfide signaling and the growth-defense trade-off in rice

Article Title: Growth or immunity? OsCBSX3’s molecular toggle decides

Article References: Pu, M., Liu, S., Xie, Y., & Chen, J. (2025). Growth or immunity? OsCBSX3’s molecular toggle decides. Crop Health, 3(1), Article 18. https://doi.org/10.1007/s44297-025-00057-0

Image Credits: AI Generated

DOI: 10.1007/s44297-025-00057-0

Keywords: rice, hydrogen sulfide, OsCBSX3, growth-defense trade-off, plant immunity, Xanthomonas oryzae, chloroplast, thioredoxin, PsbO, oligomerization, disease resistance breeding, plant signaling

The study, published in the journal Stress Biology, focuses on a long-standing puzzle in plant immunity: how the actin cytoskeleton, a dynamic meshwork of protein filaments just beneath the cell membrane, communicates with the signaling pathways that mobilize defense. Scientists have known for years that when a plant detects pathogen-associated molecular patterns, or PAMPs, through cell-surface receptors, the actin network rapidly reorganizes. Filament density, orientation and bundling all shift within minutes. Disrupting this network, whether chemically or genetically, typically leaves plants more vulnerable to infection. What remained unclear was which molecular players orchestrate the remodeling and how it connects to downstream immune outputs such as reactive oxygen species production.

To answer these questions, the team turned to the rice-Magnaporthe oryzae pathosystem, a classic model in which fungal spores land on the leaf surface, germinate, and build dome-shaped infection structures called appressoria. These structures generate enormous turgor pressure through glycerol accumulation, allowing the fungus to mechanically puncture the plant cuticle. The host cytoskeleton and cell wall at the infection site are critical barriers to this penetration, making them natural focal points for studying basal immunity.

The researchers first confirmed the importance of actin polymerization using latrunculin B, a macrolide compound derived from marine sponges that binds monomeric actin and prevents filament elongation. When seedlings of the japonica cultivars TP309 and Nipponbare were pretreated with the drug before spray inoculation with a virulent M. oryzae isolate, they became markedly more susceptible to blast, with higher concentrations producing stronger effects. Quantitative PCR revealed greater fungal growth in treated plants. The drug also broadly suppressed defense hormone pathways: genes in the salicylic acid pathway, including OsPAL1, OsICS1 and PR4, and genes in the jasmonic acid and ethylene pathways, including OsAOS2 and OsERF1, were all downregulated. In other words, a structurally intact actin network is not merely a passive barrier but an active prerequisite for full immune signaling.

That result pointed the investigators toward BUI1, also known as RMD or OsFH5, a class II formin protein previously famous for its role in rice development. Loss of BUI1 function causes bent uppermost internodes, dwarfism, wavy panicles and abnormal seeds, all traced to impaired cell elongation and disrupted cytoskeletal arrays. The protein carries three conserved domains: a PTEN domain that targets it to the chloroplast surface, a proline-rich FH1 domain that interacts with profilin to promote actin polymerization, and an FH2 domain that binds the growing ends of actin filaments. Notably, the team found that latrunculin B treatment downregulated BUI1 expression, hinting that the gene sits within the very regulatory circuit the drug perturbs.

Testing the bui1 mutant, derived from the moderately resistant cultivar Zhejing 22, confirmed the suspicion. After punch inoculation with M. oryzae, the mutant developed significantly larger lesions than wild type, and field trials in a blast nursery showed dramatically reduced resistance under natural infection pressure. Using a GFP-tagged fungal strain, the researchers tracked infection in real time and found that appressorium formation and maturation were both more efficient on bui1 leaf sheath cells, suggesting that BUI1-mediated actin organization actively impedes this critical early step of fungal invasion. BUI1 expression itself was upregulated upon fungal inoculation, consistent with a positive role in defense.

The most striking finding came when the team visualized actin filaments directly. Using fluorescent phalloidin staining and confocal microscopy, they showed that treatment with the PAMPs chitin or flg22 triggered a rapid, transient increase in actin filament bundling in wild-type leaf sheath cells within five minutes. In the bui1 mutant, this response was severely attenuated, and the baseline cytoskeleton appeared disorganized. During actual fungal infection, wild-type cells accumulated dense actin bundles around infection sites by twelve hours post-inoculation, while the mutant failed to mount this defense-associated remodeling. BUI1, the data showed, is essential for PAMP-triggered actin reorganization, placing a formin protein squarely within the earliest tier of the plant immune response.

Broad-spectrum resistance is the holy grail of crop protection, and BUI1 delivered on that front too. The mutant proved more susceptible not only to blast but also to bacterial blight, developing longer lesions after inoculation with the Xoo strain PXO99A, and to sheath blight when tested in CRISPR-generated knockout lines in the Nipponbare background. Conversely, plants overexpressing BUI1 under its native promoter showed enhanced bacterial blight resistance proportional to expression level. Time-course transcriptome analysis after Xoo infection revealed extensive transcriptional reprogramming in wild-type plants that was largely absent in the mutant, with key defense pathways, including phenylpropanoid biosynthesis, MAPK signaling and plant-pathogen interaction networks, failing to activate without BUI1.

Perhaps most intriguingly, BUI1 turned out to act downstream of ROD1, a calcium sensor previously shown to suppress rice immunity by activating catalase-mediated ROS scavenging, whose loss confers broad-spectrum resistance. When the researchers knocked out BUI1 in the rod1 background, the strong resistance of rod1 plants was significantly compromised against blast, bacterial blight and sheath blight alike, though the double mutants remained less susceptible than fully wild-type plants. Yeast two-hybrid assays detected no direct physical interaction between BUI1 and ROD1 or the ROD1-interacting catalase OsCatB, indicating the relationship is genetic rather than structural. DAB staining and hydrogen peroxide measurements showed that the double mutants accumulated lower ROS levels than rod1 alone, pointing to ROS homeostasis as the mechanistic bridge.

RNA sequencing after M. oryzae infection explained why. In the bui1 knockout background, genes encoding peroxidases and metallothioneins, including OsPOD, POXA, OsCatB, OsMT1d and OsMT1f, were strongly upregulated, while ROS-producing genes such as RbohA and RbohB were unchanged. The mutant exhibited higher peroxidase activity and correspondingly lower hydrogen peroxide accumulation. BUI1, it appears, maintains immune competence primarily by restraining ROS-scavenging pathways, allowing the oxidative burst that hallmark of pattern-triggered immunity to reach effective levels. The protein also contains intrinsically disordered regions predicted to mediate liquid-liquid phase separation, and truncated variants lacking these regions failed to undergo phase separation in vitro, suggesting that BUI1 may form biomolecular condensates that serve as organizational hubs integrating cytoskeletal dynamics with defense signaling. For breeders, the message is clear: a single formin gene links the cell’s structural skeleton, its oxidative chemistry and its hormone signaling into one coordinated defense program, and tuning that gene could yield rice lines that shrug off multiple diseases without yield penalties.

Subject of Research: The role of the rice formin gene BUI1 in coordinating actin cytoskeleton remodeling and reactive oxygen species homeostasis during broad-spectrum plant disease resistance.

Article Title: BUI1 coordinates actin cytoskeleton remodeling and ROS homeostasis to confer broad-spectrum disease resistance in rice

Article References: Lin, H., Cui, K., Wang, J., Jin, Y., Zhang, X., Lu, Y., Wu, X., Zhang, L., Liu, S., Liu, J., Li, Q., Deng, Y., Yang, W., He, Z., & Gao, M. (2026). BUI1 coordinates actin cytoskeleton remodeling and ROS homeostasis to confer broad-spectrum disease resistance in rice. Stress Biology, 6(1), Article 48. https://doi.org/10.1007/s44154-026-00321-5

Image Credits: AI Generated

DOI: 10.1007/s44154-026-00321-5

Keywords: BUI1, rice immunity, actin cytoskeleton, ROS homeostasis, Magnaporthe oryzae, pattern-triggered immunity, formin, ROD1, broad-spectrum resistance, Xanthomonas oryzae, peroxidase, plant pathology

Bacterial blight, caused by the pathogen Xanthomonas oryzae pv. oryzae, commonly abbreviated Xoo, has re-emerged as a major threat to rice production worldwide. For decades, breeders have known that most cloned resistance genes against this disease, collectively known as Xa genes, trace back to wild relatives of rice or represent recessive alleles of susceptibility genes. That pattern suggested something counterintuitive: during domestication, functional disease resistance may have been actively lost rather than gained. Because the two major rice subspecies, indica and japonica, differ markedly in disease resistance and are reproductively isolated, understanding how resistance genes evolved during subspecies formation became critical for any serious attempt to balance durable resistance with high yield in modern breeding programs.

The Nature study, led by Lin and colleagues, addressed this question through a combination of map-based cloning and genome-wide association studies covering 1,945 rice accessions. From the indica variety Shuangkezao, the researchers identified a novel nucleotide-binding site and leucine-rich repeat protein, or NLR, which they designated XA48. Functional validation using CRISPR-Cas9 knockout and complementation confirmed that Xa48 confers race-specific, lifelong resistance to Northeast Asian strains of Xoo. Unlike many known Xa genes that become effective only in adult plants, Xa48 works from the seedling stage onward, a property that greatly enhances its value for breeding applications where early infection can devastate a crop.

The molecular story behind XA48 is as elegant as it is instructive. Its cognate target is XopG, a conserved and ancient metalloprotease effector deployed by diverse Gram-negative bacteria. When Xoo injects XopG into a rice cell, the XA48 receptor binds the effector directly through its coiled coil domain and oligomerizes into a calcium-permeable resistosome channel at the plasma membrane. Calcium ions flood into the cytoplasm, igniting the immune signaling cascade that culminates in hypersensitive cell death, the hallmark of effector-triggered immunity, or ETI. This mechanism parallels the well-characterized ZAR1 and Sr35 resistosomes, which likewise function as cation channels. However, the authors caution that the high-resolution structure of the XA48-XopG complex remains unsolved, and because functional XopG orthologs are concentrated in Northeast Asian Xoo populations, XA48-mediated resistance may be geographically limited in its usefulness.

Perhaps the most surprising discovery lies downstream of XA48. Using a yeast two-hybrid screen, the team identified two vascular plant one-zinc-finger transcription factors, OsVOZ1 and its homolog OsVOZ2, as direct interactors of the receptor. These transcription factors act as repressors: they suppress jasmonate signaling and negatively regulate both pattern-triggered immunity, the cell-surface basal defense known as PTI, and XA48-mediated ETI. Upon recognizing XopG, the XA48-XopG complex promotes metalloprotease-dependent degradation of OsVOZ1 and OsVOZ2 in the nucleus. With the repressors removed, expression of the OsJAZ genes drops and jasmonate-mediated defense responses are unleashed. Whether XopG directly cleaves the VOZ proteins or recruits an endogenous rice protease or E3 ligase to do so remains an open question.

The role of VOZ transcription factors turns out to be strikingly context-dependent. In rice blast resistance mediated by the NLR receptor Piz-t, both OsVOZ1 and OsVOZ2 contribute positively to immunity, and silencing both compromises Piz-t-mediated resistance. Yet in the bacterial blight system, the same proteins act as negative regulators of basal immunity and XA48-mediated ETI. This contrast suggests that VOZ proteins function as versatile signaling hubs whose output is redirected by different NLR-effector complexes in a pathogen-specific manner, a nuance that will matter for any attempt to manipulate these factors in breeding.

The evolutionary heart of the study comes from population genomic analysis of more than 2,451 rice accessions, spanning wild rice and cultivated varieties. The data revealed a remarkable asymmetry: functional Xa48 alleles exist almost exclusively in indica and have been nearly eliminated from japonica. During domestication and improvement, the frequency of functional Xa48 rose from 7.8 percent to 24.9 percent in indica, a clear signature of positive selection. In temperate japonica, by contrast, the allele collapsed from 1.0 percent to 0.3 percent, evidence of strong negative selection. The fate of a single resistance gene thus diverged dramatically between two subspecies of the same crop species.

The explanation lies at a second locus. The OsVOZ1 gene comes in two major haplotypes, one encoding an alanine, designated OsVOZ1A, and another encoding a serine, designated OsVOZ1S. Indica retains both, whereas japonica carries almost exclusively the OsVOZ1A version. When the researchers introduced Xa48 into japonica varieties carrying OsVOZ1A, the resulting plants suffered severe reductions in seed setting and grain yield across multiple seasons and locations. No such penalty appeared when Xa48 was introduced into indica backgrounds, or into japonica lines engineered to carry the OsVOZ1S allele. In other words, combining XA48 with OsVOZ1A creates a genetic immune incompatibility that cripples reproduction, which neatly explains why japonica rice purged Xa48 during domestication: the fitness cost outweighed the defensive benefit wherever XopG-positive pathogens were rare.

This incompatibility fits a broader phenomenon known as hybrid necrosis or hybrid weakness, in which novel genetic combinations trigger autoimmunity even in the absence of pathogens. Rice offers precedents, including the two-locus Hwc1/Hwc2 interaction that causes F1 hybrid weakness through constitutive accumulation of salicylic acid and jasmonic acid and upregulation of pathogenesis-related genes. The XA48-OsVOZ1A case adds to a growing catalog in which NLR receptors, paired with incompatible genetic backgrounds, undermine reproductive fitness. It also reframes how breeders should think about resistance genes: their value depends not only on pathogen recognition but on compatibility with the host’s developmental and reproductive programs.

Crucially, the study converts this evolutionary insight into a practical breeding strategy. Lin and colleagues engineered japonica lines to co-express Xa48, which mediates intracellular ETI, together with Xa21, the famous pattern-recognition receptor gene that detects the conserved RaxX peptide and confers cell-surface PTI. The resulting Xa21Xa48 plants resisted 30 diverse Xoo strains, including those virulent against either gene alone, and showed enhanced field resistance without yield loss. By reconstituting the XA48-OsVOZ1S module, pairing a functional NLR with a reproductively compatible VOZ allele, the team restored wild-rice-like broad-spectrum resistance in a modern japonica cultivar. The findings reinforce a revised model in which PTI potentiation is indispensable for NLR-mediated immunity during bacterial infection, uniting the two major branches of the plant immune system in a single engineered module. The broader lesson, the commentators argue, is that the future of crop protection lies not in deploying single resistance genes but in deliberately reconstructing entire immune networks, guided by an understanding of how natural and artificial selection have shaped them.

Subject of Research: Asymmetric selection of the rice XA48-OsVOZ1 immune module and synthetic engineering of broad-spectrum bacterial blight resistance

Article Title: An NLR-VOZ seesaw: from asymmetric selection to synthetic broad-spectrum resistance

Article References: Su, Y., Zang, S., Sun, T., You, C., & Que, Y. (2026). An NLR-VOZ seesaw: from asymmetric selection to synthetic broad-spectrum resistance. Stress Biology, 6(1), Article 52. https://doi.org/10.1007/s44154-026-00334-0

Image Credits: AI Generated

DOI: 10.1007/s44154-026-00334-0

Keywords: rice, bacterial blight, NLR immune receptor, XA48, effector-triggered immunity, pattern-triggered immunity, Xa21, OsVOZ1, asymmetric selection, broad-spectrum resistance, growth-defence trade-off, Xanthomonas oryzae

Epigenetic control in plants operates through three principal channels: DNA methylation, histone modification, and non-coding RNAs. DNA methylation in rice occurs in three sequence contexts, CG, CHG and CHH, and is maintained by distinct enzymes. Chromomethylase3 handles CHG methylation, DNA Methyltransferase 1 manages CG methylation, and Domains Rearranged Methyltransferases catalyze CHH methylation. When a pathogen attacks, these methylation patterns shift, silencing genes that would otherwise help the invader and activating defense programs that would otherwise stay dormant. The review emphasizes that this is not a passive process; it is a dynamic, energy-conscious strategy that lets the plant balance the metabolic cost of immunity against the demands of growth.

At the heart of this regulatory architecture sits the RNA-directed DNA methylation pathway, or RdDM. In this pathway, the plant-specific RNA polymerases Pol IV and Pol V generate transcripts that RNA-DEPENDENT RNA POLYMERASE 2 converts into double-stranded RNA, which DICER-LIKE 3 then processes into 24-nucleotide small interfering RNAs. ARGONAUTE 4 binds these siRNAs and uses Pol V transcripts as scaffolds to recruit DRM2, the enzyme that lays down new cytosine methylation marks. Pathogen infection triggers the production of small RNAs that silence transposable elements, genomic parasites whose activation is linked to instability and disease susceptibility. Silencing these elements enhances resistance, and remarkably, the trait can be inherited by the next generation. In rice, the largest subunit of Pol IV is encoded by OsNRPD1a and OsNRPD1b; knocking these genes down produces dwarfed plants with increased tillering, reduced panicle length and, through a still-unknown pathway, enhanced disease resistance.

The review highlights WRKY45 as a striking example of multilayered epigenetic control. This transcription factor, a hub of quantitative resistance to bacterial blight, is regulated simultaneously by DNA methylation, histone modifications and small RNA pathways. A transposon-derived small RNA called TE-siR815 modulates the WRKY45 locus, and demethylation at that locus alters expression and, with it, susceptibility to Xoo. The authors argue that WRKY45-1 and WRKY45-2 function as molecular bridges connecting epigenetic control to the wholesale transcriptional reprogramming that defines the immune response against both bacterial and fungal attackers.

Concrete examples of methylation-driven resistance abound in the literature the review surveys. The famous resistance gene Xa21, which encodes a receptor kinase conferring defense against diverse Xoo strains, has a relative called Xa21G that was isolated through methylation-sensitive amplification polymorphism screening in a mutant line generated with the DNA methylation inhibitor 5-aza-2′-deoxycytidine. In wild-type plants the Xa21G promoter is methylated and its transcripts are undetectable, but in the demethylated mutant the gene is expressed. Similarly, the blast resistance gene Pib, which encodes a nucleotide-binding leucine-rich repeat protein, carries CG methylation at two promoter sites, and the PigmS gene is governed by demethylation of two tandem miniature transposons, MIT1 and MITE2, that balance tissue-specific transcription against yield. The de novo methyltransferase gene OsDRM2 regulates defense against M. oryzae, while OsRos1a, a repressor of silencing, is vital for resistance to bacterial leaf streak caused by Xanthomonas oryzae pv. oryzicola.

Histone chemistry adds a second, equally intricate layer. Activating marks such as trimethylation of histone H3 lysine 4 open chromatin and permit transcription, whereas repressive marks such as H3K27me3 seal genes shut. Rice possesses twenty Jumonji C domain histone demethylases, and several are now firmly implicated in immunity. JMJ704 promotes resistance to bacterial blight by removing H3K4me2/3 marks from negative regulators of defense, including OsWRKY62 and the susceptibility gene OsSWEET14. JMJ705, induced by stress and infection, strips H3K27me3 from defense and jasmonic acid-responsive genes; its overexpression produces a lesion-mimic phenotype and heightened Xoo resistance, while its loss diminishes resistance. On the acetylation side, the histone acetyltransferase OsHAC704 activates defense genes, whereas the deacetylases OsHDAC1 and OsHDT701 act as brakes. Knocking down OsHDAC1 enhances broad-spectrum blast resistance without stunting the plant, and the transcription factor OsGRAS30 boosts resistance by inhibiting OsHDAC1 and elevating H3K27ac levels. OsHDT701, working with the RNase P subunit Rpp30, deacetylates histone H4 at pattern-recognition and defense genes, dampening responses to both M. oryzae and Xoo. The sirtuin-like deacetylase OsSRT1 suppresses jasmonic acid biosynthesis genes, and its downregulation triggers lesion formation and hypersensitive-response gene expression, tying histone modification directly to hormone-mediated defense signaling.

Pathogens, for their part, have learned to weaponize the host’s epigenetic machinery. The secreted effector Uv1809 from the false smut fungus Ustilaginoidea virens enhances OsSRT2-mediated histone deacetylation, lowering H4K5ac and H4K8ac levels and crippling the transcriptional activation of defense genes. Host-induced silencing of Uv1809 restores resistance, demonstrating that fungal effectors actively suppress immunity by hijacking chromatin regulators. Other fungal and bacterial effectors induce histone hypoacetylation more broadly, underscoring an escalating arms race fought at the level of chromatin.

Non-coding RNAs form the third pillar. The microRNA miR7695 targets OsNRAMP6, and its overexpression increases blast resistance, while miR160a targets the auxin signaling component ARF16 and, when overexpressed, limits fungal growth and boosts hydrogen peroxide accumulation and defense gene expression. Conversely, M. oryzae induces miR319, which suppresses OsTCP21 and compromises jasmonic acid synthesis, a clear example of a pathogen exploiting a host microRNA. In the antiviral arena, ARGONAUTE 18 sequesters miR168, freeing AGO1 for antiviral RNA interference, and AGO1a overexpression confers resistance to Xoo. Viral infection suppresses miR528, unleashing its target L-ascorbate oxidase to generate reactive oxygen species for defense. Beyond microRNAs, RNA modifications are emerging as a frontier: the m6A methyltransferase MTA1 is essential for virulence in the blast fungus, and in rice the ac4C RNA modification, written by OsNAT10, undergoes infection-triggered changes that reprogram translation and activate jasmonic acid biosynthesis, a mechanism the review flags as a key discovery in plant immunity.

Perhaps the most consequential theme is epigenetic memory. DNA methylation patterns associated with resistance can persist for generations without the original pathogen stimulus, and rice plants exposed to M. oryzae show heritable methylation and histone changes that activate defense genes in their progeny. Methyl jasmonate-induced priming elevates H3K4 and H3K9 acetylation at defense gene promoters and creates chromatin-based memory of wounding. The review argues that this molecular memory, combined with emerging tools such as CRISPR-based epigenome editing, epi-breeding with natural epialleles, and high-throughput biomarker screening using bisulfite sequencing and ChIP-seq, could deliver broad-spectrum, durable resistance without the yield penalties that plague conventional approaches. Challenges remain, including the complexity of interacting epigenetic layers, potential off-target effects of editing systems, and the difficulty of validating biomarkers in a dynamic epigenome. But the authors are clear about the destination: identifying resistance-associated epigenetic markers and integrating them with traditional breeding and biotechnology offers a sustainable path to protecting rice, and global food security, against pathogens that will not stop evolving.

Subject of Research: Epigenetic regulation of rice immunity against bacterial and fungal pathogens

Article Title: Regulatory role of epigenetics in rice immunity against bacterial and fungal pathogens

Article References: Shah, G., Ullah, H., Chen, L., Shah, A. Z., Shaheen, R., Liu, J., & Kong, W. (2026). Regulatory role of epigenetics in rice immunity against bacterial and fungal pathogens. Crop Health, 4(1), Article 18. https://doi.org/10.1007/s44297-026-00080-9

Image Credits: AI Generated

DOI: 10.1007/s44297-026-00080-9

Keywords: rice immunity, epigenetics, DNA methylation, histone modification, non-coding RNAs, RdDM, Magnaporthe oryzae, Xanthomonas oryzae, disease resistance, epigenetic breeding, CRISPR epigenome editing, food security