The discovery, published in Nature Genetics, marks only the second insect resistance gene ever cloned in wheat and just the eleventh across all of plant science. The scarcity of cloned insect resistance genes reflects genuine technical obstacles. While more than 450 resistance genes have been cloned in crops over the past three decades, roughly 70 of those within the Triticeae tribe alone, nearly all encode canonical nucleotide-binding leucine-rich repeat proteins that defend against fungi, oomycetes, bacteria and viruses. Insect resistance phenotyping is laborious and unpredictable, and the molecular mechanisms underlying plant-aphid interactions remain poorly resolved. The Gb3 clone now offers a rare genetic foothold into that underexplored territory.

The greenbug, Schizaphis graminum, is a formidable adversary. It feeds on 70 species within the grass family, vectors the devastating barley yellow dwarf virus, and has caused as much as US$100 million in losses during severe outbreaks in the American Great Plains. The pest is also extraordinarily diverse, with about 50 biotypes identified in the United States, and the continuous emergence of new virulent biotypes regularly erodes the durability of crop resistance. Six greenbug resistance genes had been mapped to chromosome 7D of Aegilops tauschii, the diploid wild relative that contributed the D genome to bread wheat, but none had been molecularly identified since Gb1 was first described in the 1950s. Among them, Gb3 stood out for its remarkable breadth: it confers resistance to 26 of 47 previously tested greenbug biotypes.

To clone the gene, the team deployed a genome-wide association study on a panel of 260 Aegilops tauschii accessions that had been evaluated for resistance to four greenbug biotypes, C, E, I and TX1. The mapping narrowed the locus to a 300-kilobase interval on chromosome arm 7DL. Collinearity analysis across pangenome sequences of resistant and susceptible accessions then revealed a decisive pattern: extensive deletions of 155 to 180 kilobases swept through the interval in every susceptible accession, while a single annotated gene, AetT093_7Dv1G1086000, was consistently present in all resistant lines and completely absent in all susceptible ones. That gene was Gb3. Haplotype analysis across the panel confirmed the association, with Gb3 detected in 100 percent of resistant accessions and missing from 98 percent of susceptible ones, and with eight distinct haplotypes identified among the carriers, the most common of which appears concentrated in Afghanistan, Turkmenistan and Iran, hinting at the gene’s centers of origin.

What the gene encodes proved to be the study’s biggest surprise. Gb3 produces a 603-amino-acid protein with two kinase domains joined by flexible linkers: a conventional protein kinase-like domain and a mitogen-activated protein kinase kinase kinase-like domain, the latter a configuration not previously seen in any cloned plant resistance gene. Comparative analysis against the eleven cloned tandem kinase proteins showed only 20 to 36 percent sequence identity, underscoring how unusual Gb3 is. The protein carries all nine essential conserved residues in its kinase-like domain but only eight in the MAP3K-like domain, a signature of a kinase-pseudokinase pair. Biochemical assays bore this out. Recombinant proteins containing the kinase domain autophosphorylated in vitro, shifted on Phos-tag gels and incorporated radioactive phosphate from labeled ATP, while the pseudokinase domain showed no such activity. AlphaFold2 modeling revealed a modular two-domain structure with an extended beta-finger motif in the active domain, a feature implicated in effector recognition by other tandem kinases. Fluorescent tagging in wheat protoplasts localized the protein to the cytosol, confirming that Gb3 operates as an intracellular receptor.

Functional validation followed the gold standard of plant genetics. The researchers cloned the full 16.1-kilobase genomic fragment, including its native promoter and terminator, and introduced it into the susceptible wheat cultivar Fielder. Complemented lines gained resistance to all eight greenbug biotypes tested, matching the resistant control TAM112, and showed no penalty across seven agronomic and yield traits. In the reverse experiment, CRISPR-Cas9 knockouts of Gb3 in TAM112 turned susceptible to four of five biotypes tested. The one exception, biotype C, was explained by the presence of a second resistance gene, the rye-derived Gb2, which the team confirmed by PCR marker and sequencing. Together, the gain-of-function and loss-of-function results leave little doubt that this dual-domain kinase is the molecular engine of greenbug resistance.

Evolutionary analysis added a deep-time dimension. Searching 270 publicly available plant genomes across 52 monocot species, the team found Gb3 orthologs exclusively within the Triticeae tribe, in Aegilops tauschii, Aegilops sharonensis, Aegilops longissima, Aegilops speltoides and Thinopyrum intermedium. The two kinase domains themselves have separate histories: the kinase II domain is present across all grasses, while kinase I first appears in barley. Their pronounced divergence implies that Gb3 was born from the fusion of two protein domains, an event the authors estimate occurred between 7.3 and 11.6 million years ago, with subsequent duplication and indel events shaping the gene’s distribution. Notably, the six greenbug resistance genes previously mapped to chromosome 7D of Aegilops tauschii, Gb3, Gb4, Gb7, Gb8, Gb9 and Gb49921, all encode identical proteins, meaning they are the same gene independently named in different genetic backgrounds. Functional allelic variants were also identified in the other Aegilops species, and a diagnostic PCR marker developed in the study should accelerate breeding efforts.

The mechanism of resistance emerged from histological, transcriptomic and metabolomic profiling at four time points after greenbug infestation. Staining for hydrogen peroxide revealed that susceptible plants mount a prolonged and excessive oxidative stress response, with significantly elevated accumulation at feeding sites and surrounding cells at four and eight days post infestation. Resistant plants, by contrast, hosted far fewer feeding sites, indicating that Gb3 deters the insects before extensive damage occurs. Transcriptomics showed that susceptible plants activate genes tied to oxidative stress, hydrogen peroxide catabolism, glutathione metabolism and iron homeostasis, essentially scrambling to manage the damage. Resistant plants expressing Gb3 instead switched on genes for systemic acquired resistance, salicylic acid and abscisic acid responses, and, critically, the biosynthesis of oxylipins, monoterpenes, flavonoids and terpenoids within a single day of infestation.

Metabolomics reinforced the picture. Susceptible plants accumulated alkaloids, flavonoids and amino acids after attack, defenses the aphids apparently detoxify or sequester. Resistant plants showed marked increases in terpenoids, lipids and phenolic acids, particularly at eight days, with diterpenoids and sesquiterpenoids prominent among the terpenes and free fatty acids feeding a sustained oxylipin pipeline. These compound classes are well known for their repellent and insecticidal properties: volatile monoterpenes and sesquiterpenes can repel or intoxicate insects, diterpenes can disrupt cell membranes, and oxylipins such as jasmonic acid and its precursors suppress insect growth. Intriguingly, Gb3 appears to rely on jasmonic acid signaling rather than the salicylic acid pathways typical of many pathogen resistance genes, distinguishing it from canonical NLR-mediated immunity and aligning it with the peculiar biology of phloem-feeding aphids.

The working model that emerges is elegant. Gb3, sitting in the cytosol as a kinase-pseudokinase receptor, likely recognizes a greenbug effector protein delivered during feeding, with the pseudokinase domain possibly serving as a decoy that facilitates binding. Recognition then triggers transcriptional and metabolic reprogramming that floods the plant with defensive oxylipins, terpenoids and phenolic acids while repairing cell walls and priming systemic signals. When recognition fails, greenbugs suppress basal immunity, neutralize defensive metabolites and exploit oxidative stress to induce premature leaf senescence, remobilizing nutrients for their own benefit. The practical implications are immediate: with the gene cloned, a diagnostic marker in hand, and transgenic Gb3 expression shown to confer broad resistance without agronomic cost, breeders now have a powerful tool for stacking durable aphid resistance into cereal crops. As greenbug biotypes continue to evolve and climate pressures intensify insect outbreaks worldwide, a single ancient fusion protein from a wild grass relative may prove to be one of wheat’s most valuable inherited assets.

Subject of Research: Cloning and mechanism of the Gb3 insect resistance gene in wheat

Article Title: Gb3 encodes a unique kinase fusion protein conferring greenbug resistance in wheat

Article References: Lhamo, D., Shen, J., Li, G., Mohr, T., Thilmony, R., Chotewutmontri, P., Chang, H.-C., Ye, H., Luo, M., Liu, S., Bai, G., Rudd, J., Carver, B. F., Gu, Y. Q., Xu, X., & Xu, S. S. (2026). Gb3 encodes a unique kinase fusion protein conferring greenbug resistance in wheat. Nature Genetics, 58(10), 2696-2705. https://doi.org/10.1038/s41588-026-02754-0

Image Credits: AI Generated

DOI: 10.1038/s41588-026-02754-0

Keywords: wheat, Gb3, greenbug, aphid resistance, kinase fusion protein, Aegilops tauschii, plant immunity, CRISPR, oxylipins, genome-wide association study, Triticeae, crop breeding

The research team set out to answer a question that has long frustrated plant pathologists and viticulturists alike: why do some grapevine cultivars tolerate infection by trunk disease fungi while others succumb, even though no grapevine genotype is fully resistant? Tolerance in this context is measured by the expression of foliar symptoms, which varies considerably among cultivars, yet the biochemical mechanisms underlying this variation have remained poorly understood. To probe the question, the researchers chose two cultivars with well-documented contrasting responses to Botryosphaeria dieback: Chardonnay, which shows greater tolerance, and Gewurztraminer, which is more susceptible. By comparing how these two cultivars reconfigure their chemistry after infection, the team hoped to identify the metabolic signatures that separate a resilient vine from a vulnerable one.

The experimental design was ambitious in scope. Rather than examining only the infection site in the woody stem, as most earlier studies have done, the researchers conducted whole-plant metabolomic analyses, sampling wood, leaves and roots at different times after inoculation. They used untargeted liquid chromatography coupled with mass spectrometry, a technique that allows scientists to detect and measure thousands of small molecules simultaneously without knowing in advance which ones will prove important. This unbiased approach is critical when studying complex plant-pathogen interactions, because defense chemistry often involves unexpected compounds and pathways that a targeted analysis would miss entirely.

A key feature of the study was the use of two different N. parvum isolates that differ in aggressiveness. Pathogen colonization assays confirmed that the two isolates possessed contrasting wood invasion capacities, with one spreading more extensively through the host tissue than the other. This distinction mattered: it allowed the researchers to separate the effects of the plant cultivar from the effects of the fungal strain, revealing that the outcome of infection depends on the specific pairing of host and pathogen rather than on a generic interaction between grapevine and wood-decay fungus. The two isolates used in the work were designated Np.Bt67 and Np.Bourgogne, and their differing behavior in the wood provided a natural experiment in fungal virulence.

When the team analyzed the resulting metabolomic data using principal component analysis, a statistical method that reveals the dominant sources of variation in large datasets, a clear pattern emerged. The cultivar of the vine and the identity of the fungal isolate were the main factors structuring metabolic variation across the experiment, with additional contributions from the organ being sampled and the time elapsed since inoculation. In other words, the chemical state of a vine after infection is not determined by the fungus alone or the plant alone, but by the interplay between a particular cultivar and a particular fungal isolate, modulated by where in the plant one looks and how long the infection has had to develop.

The most striking differences appeared in the wood, the primary battleground between vine and pathogen. In response to the most aggressive isolate, the two cultivars mounted clearly distinct metabolic responses, particularly in their profiles of stilbenes and oxylipins. Stilbenes are a family of phenolic compounds, including the famous resveratrol, that grapevines synthesize as antifungal weapons, and their production is governed by enzymes such as stilbene synthase and the upstream phenylalanine ammonia-lyase, both central players in plant defense. Oxylipins, by contrast, are oxygenated derivatives of fatty acids produced through the lipoxygenase pathway, and they serve as both antimicrobial compounds and signaling molecules that coordinate defense responses across the plant.

Here the tolerant cultivar revealed its hand. Compared with Gewurztraminer, Chardonnay showed a faster and stronger induction of stilbene and fatty acid synthesis in its wood, especially of oxylipins, compounds that could be involved in both direct defense and long-distance signaling. This rapid chemical mobilization suggests that the tolerant vine does not simply produce more of the right compounds at the end of the battle; it activates its defensive chemistry earlier and more vigorously, potentially slowing the pathogen before it can establish a firm foothold. Notably, the study found that pathogen growth was similar between the two cultivars, meaning that the difference in tolerance cannot be explained by the fungus simply growing more slowly in Chardonnay. Instead, the two cultivars are characterized by specific metabolite signatures, especially in the wood, pointing to fundamentally different interaction mechanisms rather than a common response to wood decay.

Perhaps the most surprising finding came from beyond the infection site. The researchers observed that leaves and roots also exhibited early metabolic adjustments after the fungus was introduced into the wood, and these systemic changes were more pronounced in Chardonnay than in Gewurztraminer. This indicates that the tolerant cultivar mounts a rapid whole-plant response, reprogramming its metabolism far from where the pathogen is actually attacking. Such systemic metabolic reprogramming may reduce the overall impact of infection on host tissues, priming distant organs to cope with the physiological disruption that trunk disease causes as it progresses. The finding challenges the conventional focus on the wood alone and suggests that the fate of an infected vine is decided, in part, by how quickly the entire plant can reorganize itself.

The broader implications of this work extend into viticulture and breeding. Grapevine trunk diseases are increasingly concerning in the context of climate change, and with no fully resistant genotypes available, growers currently rely on costly and labor-intensive management practices, including the surgical removal of infected wood and the replanting of dead vines. Understanding the metabolic basis of tolerance could eventually help breeders select for cultivars with the rapid stilbene and oxylipin responses seen in Chardonnay, or guide the development of treatments that stimulate these pathways in susceptible varieties. The study also underscores that fungal isolate matters as much as host cultivar, which means that breeding and protection strategies may need to account for the local diversity of Botryosphaeriaceae populations in vineyards.

By integrating pathogen colonization data with untargeted metabolomics across three organs, two cultivars, two fungal isolates and multiple time points, the research provides a more integrated view of grapevine responses to Botryosphaeriaceae infection than has previously been available. The work, conducted at the Université de Haute Alsace with plants supplied by INRAE UMR SVQV in Colmar, France, and supported by the French Ministry of Higher Education and Research, demonstrates that tolerance to trunk disease is not a single trait but a dynamic, system-wide chemical performance. As vineyards face mounting pressure from a warming climate and evolving pathogen communities, studies like this one bring the field closer to understanding why some vines endure what destroys others, and how that resilience might one day be engineered or bred into the varieties the wine world depends on.

Subject of Research: Metabolomic responses of tolerant and susceptible grapevine cultivars to infection by the trunk disease fungus Neofusicoccum parvum

Article Title: Whole plant metabolomic analysis reveals contrasted responses in tolerant and susceptible grapevine cultivars to infection with different isolates of Neofusicoccum parvum, a major trunk disease fungus

Article References: Grau, A. L., Lacrampe, N., Goddard, M.-L., & Chong, J. (2026). Whole plant metabolomic analysis reveals contrasted responses in tolerant and susceptible grapevine cultivars to infection with different isolates of Neofusicoccum parvum, a major trunk disease fungus. BMC Plant Biology. https://doi.org/10.1186/s12870-026-09951-3

Image Credits: AI Generated

DOI: 10.1186/s12870-026-09951-3

Keywords: grapevine, Neofusicoccum parvum, Botryosphaeria dieback, grapevine trunk diseases, metabolomics, stilbenes, oxylipins, plant defense, Chardonnay, Gewurztraminer, fungal pathogen, viticulture

The logic behind the study begins with the ketogenic diet, a high-fat, very low-carbohydrate regimen that forces the body to burn fat and produce ketone bodies, chiefly beta-hydroxybutyrate and acetoacetate. These molecules serve as alternative fuel for the brain when glucose is scarce, but beta-hydroxybutyrate is more than an energy source. It is also a signaling molecule: it inhibits histone deacetylases, enzymes that silence genes, thereby boosting expression of protective factors such as brain-derived neurotrophic factor; it binds the HCAR2 receptor to dampen inflammation; and it can block assembly of the NLRP3 inflammasome, a molecular machine that drives inflammatory responses. Rodent studies have linked ketogenic diets to preserved memory, muscle mass, and physical function, and short-term ketogenic diets have improved memory in middle-aged female mice and older male rats. Human evidence, however, remains mixed, with small trials in mild cognitive impairment and Alzheimer’s disease showing modest or null effects.

Sticking to a strict ketogenic diet is difficult, particularly for older adults who may be vulnerable to nutritional shortfalls. The California team therefore turned to a supplement strategy: the ketone monoester (R)-3-hydroxybutyl (R)-3-hydroxybutyrate, known commercially as deltaG. When eaten, carboxylesterase enzymes in the small intestine split the compound into beta-hydroxybutyrate and 1,3-butanediol; the liver then converts the butanediol into additional beta-hydroxybutyrate and releases it into circulation. This raises blood ketones for several hours without severe carbohydrate restriction, allowing researchers to ask whether selected effects of a ketogenic metabolic state can be reproduced simply by elevating beta-hydroxybutyrate availability.

The experiment involved 24-month-old C57BL/6 mice, roughly equivalent in age to an elderly human, obtained from the National Institute on Aging’s aged rodent colony. At the start of the intervention, animals were randomized to a control diet or a ketone ester diet in which 21.5 percent of carbohydrate-derived calories were replaced with the ester, with vitamins, minerals, and fiber matched between groups. Each mouse received a fixed isocaloric daily ration of 12.2 kilocalories for eight weeks. Over the intervention, the researchers tracked body weight and composition by nuclear magnetic resonance relaxometry, tested spatial memory in the Barnes maze and recognition memory in the novel object recognition task, measured anxiety-like behavior in an open field, assessed motor coordination on a rotarod and grip endurance on a wire hang, and finally profiled metabolites in liver, hippocampus, muscle, serum, and urine using proton nuclear magnetic resonance spectroscopy. They also quantified 76 oxylipins, lipid messengers derived from polyunsaturated fatty acids that regulate inflammation and vascular tone, in the hippocampus.

The proximal metabolic effects were unambiguous. After seven weeks, postprandial beta-hydroxybutyrate was dramatically higher in ketone ester-fed animals of both sexes, with a very large diet effect, and postprandial glucose was significantly lower. Notably, ester-fed females reached higher blood ketone levels than ester-fed males, a sex difference consistent with prior reports that females achieve higher circulating beta-hydroxybutyrate under ketogenic feeding. The divergence began downstream. Male mice on the ester diet ended the study weighing less than at baseline, with significantly lower body fat percentage and higher lean mass adjusted for body weight, although absolute lean mass was unchanged. Females showed no comparable body composition shift, but they did display lower absolute lean mass and, intriguingly, a higher gastrocnemius muscle mass relative to body weight.

Metabolomic profiling revealed that the two sexes were essentially running different metabolic programs in response to the same supplement. In males, serum and urine metabolomes did not separate cleanly by diet in multivariate models, but individual markers pointed toward altered handling of branched-chain amino acid catabolites and nicotinamide-related metabolites, alongside higher hepatic glycine and sarcosine, intermediates of one-carbon metabolism. In females, the diet produced broad, statistically significant shifts in the serum, urine, and liver metabolomes, touching amino acids, glycolytic products, and tricarboxylic acid cycle intermediates such as fumarate, aspartate, glutamine, and glutamate, which fell in ester-fed females. The authors caution that because the ester diet also reduced starch and removed maltodextrin, and because food intake and energy expenditure were not directly measured, these changes cannot be attributed exclusively to beta-hydroxybutyrate signaling.

The cognitive results were the study’s most striking sex-specific finding. On the Barnes maze probe trial, in which mice must locate a target hole on a circular platform from memory, ester-fed females made significantly fewer primary errors than control females, an incidence rate ratio of 0.57, meaning they explored roughly 43 percent fewer wrong holes before finding the target. Males showed no such benefit. The effect was specific: recognition memory, open-field anxiety measures, and motor tests were unchanged in both sexes, and the wire hang test in females was limited by a ceiling effect, with most animals reaching the maximum 180 seconds. The authors emphasize that the Barnes maze result should be read as a task-specific change in spatial search performance rather than broad cognitive enhancement.

In the hippocampus, the molecular picture in females was suggestive but complex. Ester-fed females expressed significantly lower levels of interleukin-1 beta messenger RNA, a cytokine downstream of inflammasome activation that has been implicated in hippocampal dysfunction, while IL-18, interferon-gamma, and BDNF transcripts were unchanged. Hippocampal oxylipin profiles shifted in a mixed direction: pro-inflammatory species such as prostaglandin F2 alpha and thromboxane B2 rose alongside species often classified as anti-inflammatory or pro-resolving, including 15-oxo-ETE, prostaglandin E1, and two epoxy fatty acids. Exploratory correlation analyses showed that hippocampal beta-hydroxybutyrate was inversely associated with IL-1 beta expression, but Barnes maze errors did not correlate significantly with any of these molecular measures, so the study does not establish a causal chain from ketones to reduced neuroinflammation to better memory.

The authors are candid about limitations. The aged cohort suffered substantial attrition before and during the intervention, raising possible survivorship bias; biochemical profiling was performed only after a 12-hour fast, which likely blunted between-group ketone differences; and the ester diet differed from the control diet in carbohydrate amount and composition, not merely in ketone content. Neuroimmune endpoints were measured at the transcript level only, without protein or inflammasome activity assays. The team also notes recent work associating continuous ketogenic diet exposure with p53-dependent cellular senescence in mice, even as other studies suggest beta-hydroxybutyrate itself can mitigate senescence in several models, underscoring that diet composition, duration, and delivery method may determine whether ketone elevation helps or harms.

For now, the study stands as rigorous preclinical evidence that a ketone ester supplement can produce robust metabolic changes in aged animals while its behavioral and body-composition effects split along sex lines. The researchers call for follow-up work that disentangles ketone-specific effects from carbohydrate reduction, measures food intake and energy expenditure directly, validates inflammatory findings at the protein level, and ultimately tests whether similar sex-specific responses appear in older humans. Until then, the message for the booming ketone-supplement market is one of caution: the same molecule may mean very different things to an aging male body and an aging female brain.

Subject of Research: Sex-specific effects of ketone ester supplementation on cognition and metabolism in aged mice

Article Title: Ketone ester supplementation in aged mice produces sex-specific cognitive and metabolic effects

Article References: Roslund, K. J., Coates, L. C., Sattar Sultani, S., Hayes, D., Diaz, S., Rutkowsky, J. M., Zhou, Z., Ramsey, J. J., Taha, A. Y., & Slupsky, C. M. (2026). Ketone ester supplementation in aged mice produces sex-specific cognitive and metabolic effects. GeroScience. https://doi.org/10.1007/s11357-026-02546-8

Image Credits: AI Generated

DOI: 10.1007/s11357-026-02546-8

Keywords: ketone ester, beta-hydroxybutyrate, aging, cognition, spatial memory, hippocampus, neuroinflammation, metabolomics, oxylipins, body composition, sex differences, GeroScience

The story begins with the plastisphere, the term coined for the communities of bacteria, algae, fungi, and other microbes that rapidly form biofilms on plastic debris once it enters aquatic environments. Diatoms are consistently among the earliest and most successful colonizers of these artificial surfaces. Because plastics are buoyant, long-lived, and chemically inert compared with natural substrates, they offer diatoms a novel and stable ecological niche in the sunlit surface ocean. Field surveys from the Black Sea to intertidal habitats worldwide, along with laboratory mesocosm experiments, have repeatedly documented genera such as Chaetoceros, Thalassiosira, Skeletonema, Navicula, and Nitzschia dominating plastic-associated biofilms, sometimes outcompeting every other photosynthetic organism on the particle.

What makes this dominance ecologically significant is that many of these same diatom genera are well known as producers of oxylipins, a family of lipid-derived defensive chemicals. When diatom cells are damaged, for example when a copepod crunches them during feeding, enzymes called lipoxygenases are released and convert membrane fatty acids into a diverse array of oxylipins, including polyunsaturated aldehydes and linear oxygenated fatty acids. Decades of laboratory and field research have shown that these compounds are teratogenic to copepods: they reduce egg production, impair hatching success, and can kill nauplii outright, sometimes with devastating effects on entire cohorts. In extreme cases documented in the literature, diets rich in oxylipin-producing diatoms such as Skeletonema marinoi have led to one hundred percent naupliar mortality.

Copepods, meanwhile, occupy a pivotal position in ocean ecology. With roughly thirteen thousand described species, they can make up seventy to ninety percent of mesozooplankton abundance in many regions, forming the critical link between phytoplankton and commercially important fish, marine invertebrates, and even cetaceans. They also play a major role in the ocean carbon cycle, packing organic material into dense fecal pellets that sink rapidly and transporting carbon through their daily vertical migrations. Because copepods passively entrain particles of suitable size into their feeding currents, they readily ingest microplastics that overlap in dimensions with their natural prey such as diatoms, dinoflagellates, and ciliates.

The consequences of this ingestion are well documented. Laboratory studies have shown that exposure to microplastic concentrations as low as fifty particles per milliliter can alter copepod feeding behavior, prey selection, reproductive output, molting cycles, and lipid production. In the copepod Acartia tonsa, polystyrene beads administered during egg formation produced smaller eggs, reduced naupliar survival, and population models projecting a thirty-fold decline over twenty generations. Molecular analyses reveal that microplastic ingestion triggers oxidative stress pathways involving MAPK and Nrf2 signaling, drains cellular energy reserves, and compromises swimming performance. Fecal pellets produced by exposed copepods become smaller and sink more slowly, potentially weakening the biological pump that carries carbon to the deep ocean.

The striking observation at the heart of the new review is that these microplastic effects closely resemble those historically attributed to oxylipin-producing diatoms. Reduced egg viability, impaired hatching, naupliar mortality, and disrupted maternal investment appear in both bodies of literature. Donnarumma and Russo propose that the overlap may not be coincidental. When a copepod ingests a plastic particle densely colonized by diatoms, the mechanical crushing of those cells during digestion could liberate lipoxygenases that then react with polyunsaturated fatty acids from any of the other organisms in the gut, whether eukaryotic or prokaryotic, generating oxylipins on the spot. In effect, the plastic particle would function as a chemical weapon factory inside the grazer.

Biofouling makes this scenario more plausible rather than less. Experiments consistently show that copepods ingest aged, biofilm-coated microplastics more readily than pristine particles, apparently because microbial colonization makes the plastic smell and behave more like food. Biofilm-derived infochemicals can even act as foraging cues that attract grazers. Meanwhile, nutrient limitation, a condition that increases oxylipin production in diatoms, also drives diatoms to over-secrete adhesive extracellular polymeric substances, making their biofilms stickier and more robust on plastic surfaces. The result is a particle that is simultaneously more attractive to copepods and more chemically loaded with potential toxin producers.

The authors are careful to stress that no study has yet directly demonstrated oxylipin synthesis by epiplastic diatoms on plastic debris. Their framework remains a hypothesis, albeit one grounded in converging lines of indirect evidence. To test it, they propose a clear experimental roadmap: culture an oxylipin-producing species such as Skeletonema marinoi on plastic debris, extract and characterize the resulting metabolites using liquid chromatography with tandem mass spectrometry, and compare copepod responses to sterile versus diatom-colonized particles. Adult females would be exposed to four treatments, healthy diets, free-living diatoms, sterile microplastics, and colonized microplastics, with hatching success and gene expression serving as key endpoints. Field surveys using fine neuston nets, rather than the standard manta nets that miss the relevant size fractions, would then establish whether the mechanism operates in nature.

The stakes extend well beyond copepod physiology. If plastic-borne oxylipins compound the reproductive failures already observed in laboratory studies, population-level consequences could ripple upward through marine food webs, reducing prey availability for fish larvae and other consumers. Disruption of copepod-mediated carbon export could further alter the efficiency of the biological pump, with implications for climate-relevant biogeochemical cycles. The authors also highlight a glaring geographic bias in existing research toward the Northern Hemisphere, leaving the Southern Ocean and much of the tropics as data deserts in which the combined stress of microplastics and epiplastic chemistry remains entirely unquantified.

For now, the review reframes microplastic pollution as a dual threat: a physical and nutritional burden on grazers, and a potential vector for chemical stress generated by the living communities that plastics carry with them. Whether that second threat is real in the ocean will depend on the experimental and field campaigns the authors now call for, but the convergence of evidence they assemble makes the hypothesis one of the most intriguing new directions in marine chemical ecology.

Subject of Research: Microplastics as potential vectors of diatom-derived oxylipins affecting copepod physiology and reproduction

Article Title: Microplastics as potential vectors of diatom oxylipins and possible effects on copepods

Article References: Donnarumma, V., & Russo, E. (2026). Microplastics as potential vectors of diatom oxylipins and possible effects on copepods. Discover Ecology, 2(1), Article 11. https://doi.org/10.1007/s44396-026-00029-w

Image Credits: AI Generated

DOI: 10.1007/s44396-026-00029-w

Keywords: microplastics, plastisphere, diatoms, oxylipins, copepods, marine chemical ecology, biofilms, copepod reproduction, biological pump, marine pollution, Skeletonema marinoi, zooplankton