Viroids are among the strangest infectious agents known to science. Unlike viruses, they carry no genes at all, no proteins, no protective coat. They are nothing more than small, single-stranded, circular RNA molecules, typically ranging from about 230 to 430 nucleotides, folded into elaborate rod-like structures. Yet despite this extreme minimalism, viroids wreak havoc on crops worldwide, causing devastating diseases in potatoes, tomatoes, citrus, hops, and many other species. The potato spindle tuber viroid, or PSTVd, was the first viroid ever discovered and remains a model system for understanding how these naked RNA pathogens replicate, move through plants, and trigger symptoms. Because viroids have no protein products, conventional disease-control strategies, such as those targeting viral enzymes or coat proteins, simply do not apply. This has left a glaring gap in the plant pathologist’s toolkit.

To close that gap, the Hirosaki team turned to a technique known as SELEX, short for systematic evolution of ligands by exponential enrichment. First developed in the early 1990s, SELEX is essentially an artificial Darwinian evolution experiment conducted in a laboratory tube. Researchers start with an enormous library of random DNA sequences, in this case single-stranded DNAs of 30 nucleotides in length, and repeatedly expose them to a target molecule, here purified PSTVd RNA. Sequences that happen to stick to the target are captured, amplified, and subjected to another round of selection. Over successive rounds, the population becomes progressively enriched for molecules with the strongest binding affinity, while poorly binding sequences are washed away.

What set this study apart was the level of scrutiny applied to the evolutionary process itself. Rather than waiting until the end of the selection to examine the winners, the researchers performed next-generation sequencing on the DNA population every five rounds, at rounds 5, 10, and 15. The sequencing data revealed a textbook evolutionary trajectory: with each round, the pool of DNA sequences became both more enriched and less diverse. By the fifteenth round, the number of unique sequences in the population had collapsed to just one-eighteenth of what it had been at round five, a dramatic demonstration of convergent selection pressure at work.

From this sequencing data, the team selected sixteen sequences that ranked highly in the fifth, tenth, and fifteenth rounds, along with two sequences that were actually present at low abundance in the fifth round. These eighteen candidate aptamers were then tested for their ability to physically bind PSTVd using a pull-down assay, a technique in which the viroid RNA is immobilized and candidate DNA molecules are washed over it to see which ones stay attached. The results were telling: seven of the eighteen candidates bound either in vitro-transcribed PSTVd or native PSTVd extracted from infected tissue. Perhaps most intriguingly, the strongest binder of all came not from the highly enriched late rounds but from one of the two low-abundance sequences in round five, a reminder that sheer abundance in a SELEX pool does not always predict binding superiority. Five of the other confirmed binders were among the sequences ranked highly in the fifteenth round, validating the enrichment strategy.

But the true test of any aptamer is not whether it clings to its target in a plastic tube, but whether it can do something useful in a living organism. Here the researchers made a decision that transformed the study from a routine binding exercise into something genuinely novel. Four of the confirmed binding sequences, including one that had been previously reported in the literature, were selected for co-inoculation experiments on tomato plants. In these assays, infectious PSTVd RNA transcripts were rubbed onto tomato leaves together with the candidate aptamers, and the plants were then monitored to see whether infection took hold.

The outcome defied simple expectations. Some of the aptamers significantly inhibited PSTVd infection, reducing the frequency with which plants became diseased, essentially acting as molecular shields that interfered with the viroid’s ability to establish itself. Others did the opposite: they promoted infection, apparently making it easier for the viroid to colonize the plant. The researchers analyzed infection outcomes using survival analysis, a statistical framework borrowed from clinical research and previously applied in plant pathology to time-to-event data such as leaf abscission, treating the time until a plant became infected as the measured event.

Why would some DNA sequences help the pathogen while others hinder it? The answer likely lies in where on the viroid’s intricate RNA structure each aptamer attaches. The researchers used computational structure prediction, drawing on tools in the lineage of AlphaFold 3, to model the interaction between each aptamer and the PSTVd RNA, and found that the differentially modulating behavior correlated with the specific binding sites predicted in silico. PSTVd’s circular RNA folds into a series of structural domains with distinct functions, including a pathogenicity domain whose stability and sequence influence symptom severity, and central regions implicated in replication and systemic movement. Previous work has shown that even a single nucleotide substitution can convert PSTVd from noninfectious to infectious in tobacco, and that mutations stabilizing the pathogenicity domain suppress replication and symptom expression. An aptamer that binds over a region essential for replication or movement could plausibly block the viroid’s life cycle, while one that binds elsewhere might stabilize a transient structural conformation that facilitates infection, for example by protecting a loop region involved in host protein interactions, such as the bulged hairpin known to interact with the host protein VirP1 during systemic spread.

The implications cut both ways, and the authors are candid about this. On one hand, inhibitory aptamers represent an entirely new class of potential anti-viroid agents. If DNA sequences can be designed or selected to bind critical functional motifs on viroid RNA and block infection, they could eventually inform the development of exogenously applied protective compounds, or perhaps be expressed in transgenic plants as part of a resistance strategy. This is particularly valuable for a pathogen class against which no conventional chemical or genetic control exists. Viroids are a growing concern for global agriculture, with pospiviroids spreading through commercial pepper and tomato production and recent surveys suggesting that seed transmission may have been overestimated but that trade in ornamental hosts continues to fuel outbreaks. Japan, where the research was conducted, has experienced significant economic losses from viroid incursions, and the country’s agricultural authorities remain on high alert for newly emerged plant viruses and viroids.

On the other hand, the discovery that some aptamers enhance infection raises both a caution and an opportunity. The caution is obvious: any future attempt to deploy aptamer-based control would need to rigorously screen candidate molecules for unintended proviral effects. The opportunity is subtler but scientifically rich. Pro-infective aptamers are, in effect, tools for probing which regions of the viroid genome are vulnerable bottlenecks in the infection process. By comparing where inhibitory and enhancing aptamers bind, researchers can map the functional anatomy of a viroid with a precision that conventional mutagenesis struggles to achieve, since many viroid mutations are lethal to the pathogen itself.

It is also worth noting the methodological contribution embedded in this work. A companion protocol paper published by the same collaboration in the International Journal of Molecular Sciences laid out a high-throughput sequencing and SELEX-based workflow for selecting aptamers against PSTVd, and the current study demonstrates that workflow end to end, from a random 30-nucleotide library through iterative selection, amplicon sequencing, binding validation, and finally biological testing in planta. The sequencing datasets are available from the corresponding authors upon reasonable request, and the paper includes extensive supplementary material detailing the sequence populations and binding analyses. The work was supported by the Japan Society for the Promotion of Science, including a JSPS Postdoctoral Fellowship, a KAKENHI grant, and the J-PEAKS program for forming Japan’s peak research universities.

The broader context makes the study timely. Viroid biology is enjoying a renaissance, driven in part by metatranscriptome mining that has revealed a stunning diversity of viroid and viroid-like circular RNA agents across the biosphere, fueling speculation about their deep evolutionary origins as relics of an RNA world. Fifty years after PSTVd’s discovery opened the field, researchers are still wrestling with fundamental questions about how these minimal pathogens achieve host adaptation, subcellular targeting, and pathogenesis without a single encoded protein. The Hirosaki study adds an unexpected chapter to that story: it shows that the viroid’s folded RNA architecture, long studied as the source of its pathogenic power, is also a surface that can be recognized, bound, and manipulated by short synthetic DNA molecules. Whether that manipulation can be harnessed reliably enough to protect crops in the field remains an open question, and the authors emphasize that the mechanisms underlying both inhibition and enhancement will require further dissection. But as a proof of concept, the result is striking, a bare piece of DNA, thirty letters long, capable of deciding whether a plant falls ill or stays healthy. For a pathogen with no genes, no proteins, and no cure, that may be the most meaningful pressure it has faced yet.

Rice false smut, caused by the fungal pathogen Ustilaginoidea virens, has emerged as a major threat to rice production worldwide. This pathogen forms characteristic smut balls on rice panicles, which significantly reduce yield and grain quality. Despite the agricultural significance of this disease, the molecular machinery that allows the fungus to subvert rice development and immunity remained poorly understood until now. Xu and colleagues have bridged this knowledge gap by focusing on the pathogen’s ability to hijack the plant’s lipid signaling networks—an essential communication system that influences cellular processes including growth and immune responses.

Central to this study is the discovery that the false smut fungus secretes specific effectors that target rice lipid signaling components, notably those involved in phospholipid metabolism. Lipids, beyond their structural roles, act as critical signaling molecules modulating plant responses to environmental stimuli and pathogen invasion. By manipulating these lipid signals, the fungus creates an environment conducive to its propagation, while simultaneously hampering rice’s intrinsic defense mechanisms. The disruption to lipid signaling precipitates aberrant floret development, adversely affecting the reproductive success of the rice plant and favoring fungal colonization.

Using advanced molecular techniques such as lipidomic profiling and transcriptome analysis, the researchers mapped the dynamic changes in lipid species and gene expression during infection. They uncovered an abnormal accumulation of specific phosphatidic acids and phosphoinositides, lipids known to regulate membrane trafficking and signal transduction in plants. These alterations correlated with impaired flower tissue differentiation and a suppressed expression of key immunity genes. The study thus elucidates a direct link between lipid signal reprogramming and the dual phenotypic effects of developmental manipulation and immune evasion.

One of the intriguing findings of this research is the identification of fungal effectors that interact with rice lipid kinases and phosphatases, enzymes integral to the synthesis and turnover of lipid signaling molecules. Through these interactions, the pathogen modulates enzymatic activities, skewing lipid homeostasis to its advantage. This molecular interference leads to a breakdown in signal fidelity, weakening the plant’s ability to mount an effective defense response while diverting metabolic resources to support fungal growth.

This study has significant implications for agricultural biotechnology. Understanding the pivotal role of lipid signaling in pathogen-induced developmental disorders and immune suppression enables the design of targeted interventions. For instance, engineering rice varieties with modified lipid signaling components resistant to fungal effector binding or degradation could provide durable resistance against false smut. Similarly, novel agrochemicals that stabilize lipid signaling pathways may serve as protective agents to bolster crop health under pathogen pressure.

Moreover, the findings contribute to a broader conceptual framework regarding fungal pathogenesis in plants. The hijacking of lipid-mediated signaling cascades appears to be a convergent strategy utilized by diverse phytopathogens to manipulate host architecture and overcome immune barriers. This research thus invites comparative studies exploring similar mechanisms across other crop-pathogen systems, promising to yield universal principles amenable to translational applications in crop protection.

The methodology employed by Xu and colleagues reflects an impressive integration of interdisciplinary approaches. Utilizing state-of-the-art metabolomics, genomics, and biochemical assays, the team dissected the temporal and spatial specificity of pathogen-induced lipid signaling perturbations. Such comprehensive profiling enables a nuanced understanding of how fungal effectors orchestrate host manipulation, emphasizing the importance of systems biology in unraveling complex host-pathogen interactions.

Beyond technical insights, this study underscores the dynamic interplay between pathogen virulence strategies and host developmental pathways. The ability of the rice false smut fungus to reprogram floret morphology highlights that pathogens target not only immunity but also the developmental blueprint of their hosts. This dual manipulation challenges traditional views of plant defenses and suggests that breeding for disease resistance must also consider developmental resilience as a critical trait.

Importantly, the research team validated their findings using genetically engineered rice mutants. By knocking out or overexpressing key lipid signaling genes, they demonstrated altered susceptibility to fungal infection. Mutants with disrupted lipid kinase activity showed enhanced resistance, confirming the causal relationship between lipid signaling hijacking and disease progression. This genetic evidence solidifies the mechanistic model proposed and provides practical targets for crop improvement.

The study also addresses the evolutionary aspect of fungal adaptation. The emergence of effectors capable of manipulating lipid signaling suggests a coevolutionary arms race, where the pathogen evolves sophisticated molecular tools to circumvent host defenses while maintaining compatibility with host developmental programs. This evolutionary perspective enriches our understanding of pathogen specialization and host specificity.

On a broader scale, these insights have implications for global food security. Rice feeds over half of the world’s population, and yield losses due to false smut compromise food availability and farmer livelihoods. By illuminating the molecular underpinnings of this disease, Xu et al.’s research fosters hope for more effective and sustainable management strategies that can mitigate crop losses and stabilize food production systems in the face of emerging phytopathogens.

In conclusion, the innovative work by Xu, Jin, Zhang, and collaborators represents a landmark advance in plant pathology and molecular plant sciences. By unmasking the deceptive tactics of the rice false smut fungus in commandeering lipid signaling pathways, it opens new horizons for scientific inquiry and practical solutions. Future research building on this foundation promises to deliver resilient crops equipped with sophisticated defenses, ensuring the security of a vital food resource in an era of increasing agricultural challenges.

Subject of Research: The molecular mechanisms by which the rice false smut fungus manipulates rice lipid signaling to affect floret development and immunity.

Article Title: Author Correction: Rice false smut fungus hijacks rice lipid signalling to manipulate floret development and immunity.

Article References:
Xu, Y., Jin, J., Zhang, Y. et al. Author Correction: Rice false smut fungus hijacks rice lipid signalling to manipulate floret development and immunity. Nat. Plants (2026). https://doi.org/10.1038/s41477-026-02309-5

Image Credits: AI Generated

Fungal pathogens inhabit an environment densely populated by diverse microorganisms, including bacteria, viruses, and beneficial symbiotic microbes. These beneficial microbes play critical roles in maintaining plant health by thwarting potential pathogens and modulating immune responses. Plants invest heavily in producing a broad arsenal of metabolites that selectively recruit these protective microorganisms while deterring harmful invaders. For a pathogenic fungus, successful infection entails overcoming not just the plant immune system but also the protective microbiome that surrounds and supports the host.

Effectors have long been recognized as pivotal secreted proteins that pathogens use to suppress plant immune responses, allowing fungal colonization. However, the current study, spotlighting the plant pathogen Verticillium dahliae and its effector Vd424Y, reveals a dual role for these molecules. Apart from manipulating plant immunity, a significant subset of these effectors exerts antimicrobial activity directly against microbial competitors within the host. This duality underscores an evolutionary legacy where ancient fungal proteins were primarily weapons in microbial warfare, only later co-opted to negotiate host interactions.

The team’s pioneering research involved comprehensive biochemical and structural analyses demonstrating that up to half of the proteins secreted by fungi have the capability to disrupt or inhibit other microorganisms. This extensive antimicrobial repertoire suggests that fungi have been equipped for inter-microbial competition on a broad scale, a feature that historically predates their role as pathogens. Many of these proteins, previously uncharacterized for such activity, now emerge as key players in pathogen ecology and disease progression.

Crucially, the study reports that antimicrobial proteins with effector functions are widespread across the fungal kingdom. They are not confined to pathogenic species but also occur in non-pathogenic fungi with similar structural motifs. This widespread distribution and structural conservation imply that these molecules initially evolved as microbial antagonists, serving competitive roles in complex environments rather than functions directly related to virulence or host manipulation.

Evolutionarily, ancestral fungi did not possess pathogenic traits. Instead, their primary challenge was survival amid microbial competitors, for which they evolved antimicrobial proteins to outcompete and defend against bacteria and other microorganisms. When plants and other potential hosts evolved and became colonized by fungi, these antimicrobial proteins enabled fungal colonization by modulating the host’s associated microbiome. Over time, progressive mutations augmented these proteins’ functionalities, endowing them with the capacity to suppress host immune responses directly, marking the transition from mere microbial combat to intricate host manipulation.

Focusing on Verticillium dahliae’s Vd424Y effector, the researchers provided direct evidence of its impact on both the microbial community within plants and the plant’s immune status. Vd424Y alters the microbiota composition favoring fungal colonization and disease development. Structural modifications enable this effector to penetrate plant cells, reach the nucleus, and modulate transcriptional and immune signaling pathways. This multifaceted action orchestrates an environment conducive to fungal growth while subverting host defenses.

The dual function of effector proteins sheds light on the complex biology of fungal infections. Not only do these proteins provide an advantage during microbial competition, but they also directly subvert host immunity. This multifunctionality highlights the evolutionary ingenuity of fungi, which have fine-tuned their molecular arsenal to manipulate two fronts simultaneously — the internal immune landscape of the host and the external microbial competitors.

This insight fundamentally shifts our understanding of effector proteins. Microbial competition, long considered a peripheral aspect of fungal life, is now recognized as a core driving force in effector evolution, predating and facilitating the emergence of pathogenicity. Recognizing this evolutionary trajectory opens new avenues for research and potentially transformative strategies for managing fungal diseases.

Importantly, the team speculates that this evolutionary paradigm may extend well beyond plant pathogens. Because antimicrobial activity is a deeply conserved function in fungi, similar molecular strategies might underlie fungal infections in animals and humans. Understanding fungal manipulation of host microbiota and immune systems could revolutionize medical mycology, offering novel therapeutic targets in combating fungal diseases.

From an applied perspective, these findings hold promise for agriculture and medicine alike. By elucidating how fungal effectors perturb host-associated microbiomes, researchers can devise innovative approaches to harness or restore protective microbiota, enhancing disease resistance in crops. Additionally, the vast catalog of fungal antimicrobial proteins represents a rich, largely untapped resource for the development of novel antibiotics, urgently needed in an era of increasing antimicrobial resistance.

This landmark study, published in the reputable journal Science Advances, exemplifies cutting-edge experimental research. It combines molecular biology, evolutionary genetics, and microbial ecology to decode the multifunctionality of fungal effectors. The work underscores the complexity of host-pathogen-microbiome interactions and the evolutionary forces shaping microbial arsenals.

In sum, the discovery that fungal effector proteins evolved from ancient antimicrobial agents not only reshapes foundational concepts in plant pathology but also signals a new frontier in understanding the dynamics of microbial warfare and host manipulation. This paradigm shift offers fertile ground for future research aimed at securing plant health and combating fungal diseases broadly, including those affecting humans.

Subject of Research: Not applicable

Article Title: Plant-associated fungi co-opt ancient antimicrobials for host manipulation

News Publication Date: 29-Apr-2026

Web References: DOI: 10.1126/sciadv.aec1406

References: Science Advances, Article DOI 10.1126/sciadv.aec1406

Keywords: fungal effector proteins, antimicrobial proteins, plant pathology, microbiome, microbial competition, Verticillium dahliae, host immune system, fungal evolution, plant diseases, molecular plant-microbe interactions

Late blight remains one of the most devastating diseases affecting potato production worldwide, causing massive crop losses and threatening food security. Phytophthora infestans is notorious for its virulence and adaptability, widely recognized since the nineteenth century’s Irish Potato Famine. Despite its agricultural importance, the molecular choreography orchestrating the potato’s immune defenses against this pathogen has long eluded researchers. Traditional approaches have mainly captured bulk tissue responses, obscuring the distinct behaviors of individual cell populations. This new investigation changes that paradigm by dissecting infection responses cell by cell and position by position within the infected leaf.

Employing Stereo-seq technology, which combines spatial transcriptomics with single-cell resolution, the researchers generated a comprehensive spatiotemporal atlas detailing gene expression dynamics across individual cells in potato leaves exposed to P. infestans. This technology facilitates mapping active biological processes while retaining exact cellular locations, a feat unattainable just a few years ago. By capturing this layered molecular information, the study reveals how spatial context influences immune activation and how pathogen colonization alters the plant’s microenvironment in real-time.

The team identified and categorized the major cell types present in potato leaves, including epidermal, mesophyll, and vascular cells, each demonstrating unique immune response signatures. This remarkable cellular diversity underpinning defense strategies suggests that immunity against P. infestans is not a blanket response but rather a finely tuned orchestration with roles distributed among specialized cellular compartments. By contrasting expression profiles at multiple time points post-inoculation, the study unmasked the temporal progression of immune signaling and pathogen adaptation strategies.

One of the study’s most compelling insights is the characterization of two distinct cell populations: pathogen-targeted cells (PTCs) and their immediate neighbors, surrounding PTC cells (SPCs). By analyzing pathogen presence patterns, the researchers delineated these two groups, exposing crucial spatial heterogeneity in immune activity. PTCs, directly confronted by the invading pathogen, manifest transcriptomic programs emphasizing cell wall reinforcement and stringent regulation of redox homeostasis — mechanisms vital for halting pathogen progression. Meanwhile, SPCs appear to adopt a supportive role, coordinating systemic immune signaling that may prime or amplify defense responses beyond the immediate infection locus.

These findings suggest a sophisticated communication network within the leaf tissue, where cells not directly infected by P. infestans participate actively in molding an effective defense perimeter. The spatial segregation between PTCs and SPCs may reflect a division of labor essential for balancing resource allocation and defense efficacy. Such spatially resolved cellular cross-talk constitutes a novel conceptual framework for understanding plant immunity, illustrating the complexity of host microenvironments that have remained cryptic until now.

Delving deeper, this study also sheds light on pathogen strategies that facilitate successful colonization despite host defenses. By concurrently analyzing the pathogen’s transcriptome within individual infected cells, researchers uncovered multifaceted infection tactics deployed by P. infestans. These include manipulation of host cell metabolism, suppression of immune signaling pathways, and remodeling of the cellular microenvironment to favor pathogen proliferation. The temporal dynamics of such virulence factors highlight the pathogen’s adaptability and nuance in overcoming plant defenses.

Critically, the integration of host and pathogen transcriptomes within spatial contexts provides a window into the molecular “battlefield” during infection. This dual-organism perspective elucidates how P. infestans times and targets its effector molecules to overcome the spatially defined immune obstacles erected by different potato cell types. It also underscores the pathogen’s ability to sense and respond to local microenvironmental cues, an insight that may guide the design of next-generation resistant cultivars.

From a broader ecological and agricultural standpoint, the high-resolution map presented in this study charts novel pathways toward engineering enhanced disease resistance. By pinpointing cell types and molecular processes critical for immunity, breeders and biotechnologists can tailor interventions that reinforce or mimic these natural defense strategies. Additionally, understanding how neighboring cells amplify immune signaling opens avenues for developing systemic resistance mechanisms that provide widespread protection within the plant.

This research also exemplifies the power and promise of single-cell spatial transcriptomics as a transformative tool for plant biology. Beyond the late blight system, similar approaches could revolutionize our grasp of other devastating plant diseases and symbiotic interactions. The single-cell perspective reveals nuances of cellular identity and function otherwise concealed in bulk analyses, catalyzing the discovery of intricate biological phenomena that regulate plant health.

Importantly, these findings have immediate implications for sustainable agriculture. Late blight control often relies heavily on chemical fungicides with environmental and economic drawbacks. Insights gained from this spatially resolved transcriptomic atlas may inspire next-level strategies that harness the plant’s own immune arsenal, reducing dependence on agrochemicals and enhancing crop resilience under fluctuating environmental pressures.

Moreover, the study underscores the concept of a host’s immune landscape as a dynamic and heterogeneous microenvironment shaped by both intrinsic cell-type-specific programs and extrinsic pathogen signals. Such a paradigm challenges traditional binary views of infection and resistance, promoting an appreciation of the spatial and temporal complexity inherent in biological warfare between host and pathogen. This nuanced understanding promotes innovative thinking in plant pathology and immunology.

The exceptionally detailed gene expression data, spanning various cell types and infection stages, serve as a rich resource for future explorations. This dataset enables the identification of candidate resistance genes and molecular markers that can accelerate marker-assisted selection and genome editing applications. Importantly, it lays the groundwork for deciphering how cellular metabolism, signaling cascades, and chromatin remodeling cooperate to mount effective immune responses under pathogenic stress.

Ultimately, this pioneering study breaks new ground by revealing the spatial choreography of immunity and infection in the economically vital potato–Phytophthora infestans interaction. Its revelations extend far beyond plant pathology, offering insights into fundamental principles of host-microbe interactions applicable across biology. As stereo-seq and related technologies gain traction, the prospects for unraveling complex biological processes with exquisite precision are brighter than ever.

The fusion of spatial transcriptomics and single-cell biology epitomized in this work marks a milestone toward decoding the language of cellular communication during infection. It allows scientists to witness, in real-time and space, the unfolding drama of immunity and pathogenesis on the frontline tissues where survival is negotiated. Such knowledge sets the stage for transformative advances in crop protection, food security, and sustainable agriculture in the face of mounting global challenges.

In conclusion, the elucidation of the potato–Phytophthora infestans interaction landscape at single-cell spatiotemporal resolution not only advances our scientific understanding but promises practical dividends. By unveiling the cellular heterogeneity, spatial coordination, and dynamic responses of both host and pathogen, this landmark study redefines the boundaries of plant immunology research. The path toward durable disease resistance has become clearer, informed by a molecular atlas that captures life’s complexity in unprecedented detail.

Subject of Research:
The interaction between potato leaves and the late blight pathogen Phytophthora infestans examined through single-cell spatial and temporal transcriptomics.

Article Title:
Host microenvironment in potato–Phytophthora infestans interaction revealed by single-cell spatiotemporal transcriptome.

Article References:
Li, Y., Dai, J., Dong, Z. et al. Host microenvironment in potato–Phytophthora infestans interaction revealed by single-cell spatiotemporal transcriptome. Nat. Plants (2026). https://doi.org/10.1038/s41477-025-02181-9

Image Credits:
AI Generated

DOI:
https://doi.org/10.1038/s41477-025-02181-9