The modification in question is lysine succinylation, a post-translational change in which a succinyl group is chemically attached to a lysine amino acid residue on a protein. Lysine succinylation is known to influence metabolism and transcription in a range of organisms, and previous work had charted its behavior during rice development. What remained largely unexplored was whether this modification plays a role in biotic stress — the umbrella term for damage inflicted on plants by living attackers such as viruses, bacteria, and insects. The new research, led by Lei Yang and Shuai Li together with colleagues at Yangzhou University, the Jiangsu Academy of Agricultural Sciences, and Anhui Normal University, demonstrates that it does, and in strikingly consequential ways.

To probe the question, the team performed quantitative succinylome profiling, a mass-spectrometry-based survey that measures lysine succinylation across thousands of proteins simultaneously. They applied the technique to rice plants subjected to viral infection and to herbivore infestation, and the results revealed extensive, stress-responsive succinylation on both histone and non-histone proteins. The modification preferentially decorated highly abundant proteins and was concentrated in pathways tied to photosynthesis and core metabolism. Notably, the data showed that herbivore attack increased lysine succinylation while suppressing the expression of photosynthetic pathway-related proteins, hinting that the modification tracks the metabolic reorganization plants undergo when under attack.

A central technical achievement of the study was the application of CUT&Tag analysis — a genome-mapping method that pinpoints where a particular histone modification sits along the chromosomes — to lysine succinylation in rice. The mapping showed strong enrichment of the mark at the promoters of defense-related genes, particularly genes involved in plant hormone signal transduction. Crucially, the researchers found a positive correlation between lysine succinylation occupancy at these regulatory regions and the expression levels of the corresponding genes. In other words, when the succinyl mark was present at a gene’s promoter, that gene was more likely to be actively transcribed. This positions lysine succinylation not as a passive byproduct of cellular chemistry but as an active participant in defense-related transcriptional control.

Because a modification’s abundance reflects a balance between the enzymes that add it and those that remove it, the team went hunting for desuccinylases — enzymes that strip succinyl groups from lysine residues. Working in rice, they identified three histone deacetylases as major desuccinylases: OsSRT702, OsHDA714, and OsHDA716. The researchers purified an OsHDA714-His fusion protein and validated its desuccinylation activity in vitro, confirming that the enzyme could directly remove the mark. They also generated CRISPR/Cas9-mediated knockout mutations in the corresponding genes and verified the edits by DNA sequencing, providing a clean genetic system in which to test the enzymes’ biological roles.

The functional results were dramatic. Disrupting OsHDA714 markedly enhanced rice resistance to rice stripe virus and rice black-streaked dwarf virus, two important viral pathogens of the crop, and also to the brown planthopper and the striped stem borer, two of the most destructive insect pests in rice-growing regions. A single gene knockout thus broadened resistance across two viral and two insect attackers, a breadth that conventional single-resistance breeding rarely achieves. This pattern suggests that OsHDA714 normally functions as a negative regulator of immunity — a brake on the plant’s defensive responses — and that releasing the brake, by removing the enzyme, activates a wider defense program.

To understand what that defense program consists of, the researchers integrated transcriptomic data with their CUT&Tag maps. Genes upregulated in the hda714 knockout mutant turned out to be predominantly enriched in the phenylpropanoid biosynthesis pathway, a metabolic route that produces an arsenal of antimicrobial and anti-herbivore compounds, and many of these genes carried lysine succinylation marks in their promoter regions. In parallel, jasmonate-associated defense pathways were activated in the mutant. Jasmonates are plant hormones best known for orchestrating responses to wounding and herbivory, and their involvement links the epigenetic machinery of succinylation directly to classical hormonal defense signaling. Phytohormone measurements in the mutant and in wild-type ZH11 plants supported this remodeling of hormone pathways.

Taken together, the results sketch a coherent mechanistic model. Under normal conditions, OsHDA714 — aided by OsSRT702 and OsHDA716 — keeps lysine succinylation levels in check, limiting succinyl marks at defense gene promoters and thereby restraining the expression of hormone-signaling and phenylpropanoid genes. When viruses or herbivores attack, this regulation is perturbed, succinylation accumulates on histones and key metabolic proteins, and defense transcription is reprogrammed. Removing OsHDA714 genetically locks the system into a primed state, in which the plant constitutively deploys the biochemical tools needed to fend off a diverse range of attackers. The authors propose that OsHDA714-mediated desuccinylation modulates hormone signaling and phenylpropanoid metabolism to control broad-spectrum resistance in rice.

The study carries practical implications for crop protection. Rather than stacking individual resistance genes against specific pathogens — a strategy that pathogens and pests frequently circumvent — agricultural scientists could target a regulatory hub like OsHDA714 to bolster multiple defenses simultaneously. Because the work was performed with genome editing tools such as CRISPR/Cas9, the pathway from discovery to improved germplasm is conceptually straightforward, although field performance, agronomic trade-offs, and potential effects on growth and yield would need careful evaluation, since defense activation often competes with productivity. More broadly, the research expands the known repertoire of histone modifications that regulate plant immunity, positioning lysine succinylation alongside better-characterized marks such as acetylation and methylation as a genuine epigenetic regulator of defense. It also raises questions for future work: how the cell senses viral or herbivore attack and translates it into altered succinylation, what non-histone succinylated proteins contribute to the response, and whether parallel systems operate in other crops. For now, the study provides the clearest evidence yet that a chemical tag on rice histones sits at the heart of the plant’s ability to defend itself against some of agriculture’s most persistent enemies.

Subject of Research: Role of lysine succinylation in rice defense responses against viral pathogens and herbivorous insects

Article Title: Lysine succinylation mediates defense responses against viruses and herbivores in rice

Article References: Yang, L., Li, S., Deng, X., Zhao, R., Meng, Y., Li, C., Qin, L., Liu, B., Sun, Y., Fang, J., Ji, R., & He, Z. (2026). Lysine succinylation mediates defense responses against viruses and herbivores in rice. Genome Biology. https://doi.org/10.1186/s13059-026-04271-z

Image Credits: AI Generated

DOI: 10.1186/s13059-026-04271-z

Keywords: rice, lysine succinylation, histone modification, OsHDA714, plant immunity, rice stripe virus, brown planthopper, jasmonate signaling, phenylpropanoid biosynthesis, CUT&Tag, CRISPR/Cas9, epigenomics

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: BUI1 coordinates actin cytoskeleton remodeling and ROS homeostasis to confer broad-spectrum disease resistance in rice. (n.d.). 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

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: Regulatory role of epigenetics in rice immunity against bacterial and fungal pathogens. (n.d.). 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