Most of what we know about interactions between bacterioplankton and eukaryotic plankton has come from snapshots taken during phytoplankton blooms, dramatic events in which algae multiply rapidly and then collapse. Those studies gave the impression that bacterial and algal communities link up mainly during these bursts of productivity. But whether such coupling holds up under the ordinary, day-to-day variability of the seasons—and what bacterial traits might sustain it—remained open questions. To find out, a team led by Xiao Ma and Jia Luo of the South China Sea Institute of Oceanology sampled coastal seawater over a full annual cycle, tracking how microbial communities changed from February through November.

The study’s design hinged on a crucial distinction in marine microbiology: the separation of particle-attached prokaryotes, those living on surfaces larger than three micrometers, from free-living prokaryotes, those drifting in the water between 0.2 and three micrometers. The researchers combined three complementary approaches: profiling communities using 16S and 18S rRNA gene sequencing to catalog bacteria and eukaryotes respectively, building statistical association networks to map which organisms tend to co-occur, and applying genome-resolved metagenomics to reconstruct the actual genetic blueprints of the bacteria involved.

The first major finding concerned diversity. The diversity of particle-attached bacteria rose and fell in tight synchrony with the diversity of eukaryotic plankton, showing a statistically significant positive correlation with a Pearson’s correlation coefficient of 0.459. Free-living bacteria, by contrast, maintained comparatively stable diversity through the year and showed only a weak, statistically insignificant coupling to eukaryotic diversity, with a coefficient of just 0.194. In other words, when the eukaryotic plankton community shifted with the seasons, it was the particle-attached bacteria that shifted with them, while their free-living counterparts marched to a more independent rhythm.

Network analysis reinforced this picture on a much grander scale. When the researchers mapped the statistical associations between bacterial and eukaryotic taxa, the particle-attached communities produced more than 2.5 million positive links with eukaryotes, against only about 15,000 negative links. The free-living networks, while still substantial, yielded fewer positive associations—roughly 1.45 million—and slightly more negative ones. This imbalance, with positive associations overwhelmingly dominating in the particle-attached world, points to recurrent facilitation: bacteria on particles and eukaryotic plankton repeatedly appearing together in ways that suggest mutual benefit rather than competition, and doing so consistently across the seasonal succession of species.

What might underlie this facilitation? Functional comparisons of gene content offered clues. The particle-attached communities were enriched in seven KEGG pathways, standardized categories of metabolic function, hinting at a broader capacity for carbon and nitrogen processing, enhanced energy conservation, and an increased ability to biosynthesize antibiotic- and toxin-like secondary metabolites. These chemical weapons may help particle dwellers defend their cramped, contested territories against rivals, while their expanded metabolic repertoire allows them to exploit the rich but chemically complex organic matter that particles provide.

The most striking evidence came from the reconstruction of genomes. From the metagenomic data, the team recovered 120 high-quality metagenome-assembled genomes, or MAGs, each exceeding ninety percent completeness with less than five percent contamination. The particle-attached genomes were significantly larger than their free-living counterparts, carrying more genetic real estate. When the researchers compared phylogenetically matched pairs—close relatives of the same bacterial lineages, one attached to particles and one free-living—the particle-attached members consistently showed expansions in genes for chemotaxis, the ability to swim toward chemical cues; biofilm formation, the construction of sticky surface communities; secretion systems that move molecules across cell envelopes; polymer-processing enzymes that break down complex organic matter; respiratory flexibility that allows energy generation under varying conditions; and detoxification functions for surviving chemical stress.

These near-neighbor comparisons carry an evolutionary message. Because the paired genomes are closely related, the differences between them are unlikely to reflect ancient lineage history and instead point to habitat-driven genomic divergence. Life on a particle, the authors argue, imposes persistent selection in a patchy, competitive microhabitat. Particles are islands of opportunity: rich in nutrients but crowded with competitors and short-lived in the water column. Bacteria that colonize them are favored if they can find the particles quickly, cling to them, dismantle their polymers, outcompete neighbors chemically, and adapt their metabolism to fluctuating oxygen and energy availability. The genes enabling these behaviors are costly to maintain, so free-living lineages that never encounter such pressures tend to lose or never acquire them.

Taken together, the network and genomic results support what the researchers describe as a niche-based interpretation of plankton ecology. Eukaryote-derived particles act as persistent microhabitat interfaces—tiny, ephemeral worlds that increase the heterogeneity of the seemingly uniform ocean and act as ecological filters, selecting for a particle-adapted interaction toolkit among bacteria. Because eukaryotic plankton continuously generate these particles through feeding, excretion, and decay, the bacterial communities that specialize in them remain coupled to their eukaryotic hosts year-round, regardless of whether a bloom is underway. This reframing matters because the ocean’s biological carbon pump—the process by which organic carbon is transported from the surface to the deep sea—depends heavily on particles, and the microbes attached to them determine how much carbon is recycled versus exported. Understanding that the bacteria on these particles are not passive hitchhikers but genetically specialized, persistently coupled partners adds a new dimension to models of marine food webs and carbon cycling, and suggests that the seasonal rhythm of plankton communities is underwritten by a far more intimate bacterial partnership than previously appreciated.

Subject of Research: Particle-mediated coupling between prokaryotic and eukaryotic plankton communities in coastal seawater

Article Title: Networks and genome-resolved analyses reveal persistent particle-mediated coupling between prokaryotes and eukaryotic plankton

Article References: Ma, X., Luo, J., Wu, Y., Dai, S., Wang, M., & Li, C. (2026). Networks and genome-resolved analyses reveal persistent particle-mediated coupling between prokaryotes and eukaryotic plankton. Microbiome. https://doi.org/10.1186/s40168-026-02528-0

Image Credits: AI Generated

DOI: 10.1186/s40168-026-02528-0

Keywords: particle-attached prokaryotes, free-living prokaryotes, eukaryotic plankton, association networks, genome-resolved metagenomics, metagenome-assembled genomes, marine microbiome, South China Sea, seasonal succession, chemotaxis, biofilm formation, biological carbon pump

The findings come from a team led by Hsin-Yu Wang, Chun Ming How, Yong-Shan Li, Yuqing Mao, Thanh H. Nguyen and Chia-Cheng Wei, who set out to answer a question that has become increasingly urgent in food safety research: do non-antibiotic chemicals, particularly the fungicides sprayed widely on fruit and vegetable crops, push bacteria toward resistance or heightened virulence? Prior work has hinted at the danger. Azoxystrobin and carbendazim have been shown to enrich bacterial resistomes in nematode guts, tebuconazole can promote the spread of multidrug-resistant plasmids in soil bacteria, and chlorothalonil facilitates metabolic adaptation in soil microbial communities. But whether such exposure produces phenotypic resistance and increased pathogenicity in a major foodborne pathogen remained largely untested.

Bacillus cereus was an obvious candidate for scrutiny. The Gram-positive, spore-forming organism is found in 36 to 45 percent of dairy products, vegetables, beans and cereals, and it is capable of causing food poisoning, eye infections, anthrax-like progressive pneumonia, fulminant sepsis and central nervous system infections. Multidrug-resistant strains of the species have already emerged in hospital wastewater, and its versatility—including the ability to build biofilms of varied architecture—makes any shift in its behavior a serious public health concern.

The researchers first screened eight widely used fungicides against B. cereus: chlorothalonil (CHT), propineb (PRO), tebuconazole (TEB), azoxystrobin, propiconazole, mancozeb, carbendazim and triadimefon. Three of them—CHT at 8 micromolar, TEB at 500 micromolar and PRO at 175 micromolar—completely inhibited bacterial growth within 24 hours and were selected for long-term adaptation experiments. The design was demanding: every day for 30 days, the bacteria endured a three-hour fungicide challenge followed by recovery and regrowth in fresh medium. Survival trajectories differed by compound. Under chlorothalonil, survival dipped to about 70 percent on day one but rebounded within 24 hours. Tebuconazole initially halved the population before recovery stabilized around day eight. Propineb proved the harshest pressure, dropping survival below five percent on day six before the bacteria clawed back to stable levels by day twelve. The bacterium, in short, adapted to all three chemical regimes.

Whole-genome sequencing of the adapted lineages delivered a surprising verdict: no meaningful genetic mutations. Phylogenetic comparison against reference strains and variant-calling analyses found the treated bacteria essentially identical to their ancestors. Instead of classical, mutation-driven resistance, the adaptation appears to be physiological—a reversible, non-heritable tolerance state akin to the persister-cell and stress-response phenomena documented in bacteria subjected to repeated antibiotic cycles. Similar patterns have been reported when Listeria monocytogenes and uropathogenic Escherichia coli were exposed to disinfectants such as benzalkonium chloride and triclosan, with minimum inhibitory concentrations rising without stable genetic change.

The phenotypic consequences, however, were substantial. Biofilm formation—often a shield against both immune attack and antimicrobial agents—was initially suppressed during early exposure but rose significantly in tebuconazole-adapted bacteria from day ten onward and climbed markedly in propineb-exposed cells by day ten. Statistical testing confirmed significant effects of the fungicide treatment, the duration of exposure, and their interaction on biofilm output. Antibiotic challenge assays revealed a parallel erosion of susceptibility. Bacteria adapted to chlorothalonil grew significantly better than controls in gentamicin at 4, 6 and 8 micrograms per milliliter; tebuconazole- and propineb-adapted lineages also outgrew controls at key gentamicin doses, and chlorothalonil- and tebuconazole-adapted cells showed improved growth at 8 micrograms per milliliter of tetracycline. Because no growth occurred at concentrations of 16 micrograms per milliliter or above, the strains do not meet formal clinical criteria for resistance—but the shift toward tolerance was clear and reproducible.

The most dramatic result emerged in living hosts. Using the nematode Caenorhabditis elegans, a genetically tractable infection model whose intestinal epithelium provides a biologically meaningful readout of colonization and killing, the team measured how fungicide-adapted bacteria fared against unadapted controls. All three adapted lineages killed worms significantly faster than the parent strain, with log-rank tests showing p values below 0.001. Tebuconazole-adapted bacteria were especially aggressive: worm survival collapsed within two days, and by day three most of the animals were dead. Follow-up colonization assays showed that tebuconazole-adapted B. cereus also established significantly higher intestinal loads in the worms, indicating that the fungicide had promoted persistence within the host gut, not merely faster killing.

Transcriptional profiling of the tebuconazole-adapted lineage offers a mechanistic window into these changes. Quantitative real-time PCR revealed significantly elevated expression of genes encoding the non-hemolytic enterotoxin (nheC) and the hemolysin BL complex (hblA, hblC and hblD)—toxins that disrupt intestinal epithelial cells—alongside upregulation of purC and purL, which support purine biosynthesis and extracellular DNA release during early biofilm formation, and calY, a bifunctional matrix protein that promotes adhesion to host tissues. The efflux-pump gene smr was also induced, a plausible explanation for the reduced antibiotic susceptibility, and one that echoes efflux upregulation seen in stressed Mycobacterium tuberculosis. Importantly, the elevated virulence and resistance gene expression persisted even when the adapted bacteria were subsequently exposed to gentamicin, suggesting that the stress-adapted state complicates antibiotic treatment rather than simply surviving it.

The authors are careful to frame the work as hazard identification rather than a direct portrait of what happens on farms or in food. The experiments used a single reference strain, BCRC15850, and the exposure concentrations—particularly 500 micromolar tebuconazole and 175 micromolar propineb—exceed the residue levels typically reported on treated foods, although the chlorothalonil dose is of the same order of magnitude as residues found in some food commodities. Local bioavailable concentrations in soil and produce depend on moisture, adsorption, formulation and degradation, so the laboratory model of recurrent acute stress cannot be directly translated into field-level risk estimates. Nor should the transcriptional findings be generalized beyond the tebuconazole lineage without confirming that chlorothalonil- and propineb-adapted bacteria share the same regulatory program. Nonetheless, the study reveals an understudied scenario in which persistent sublethal chemical stress can harden a major foodborne pathogen—improving its resilience, deepening its virulence and weakening the grip of frontline antibiotics—without any mutational fingerprint. Whether such phenotypes persist after fungicide withdrawal, and whether they arise in the genetically diverse field isolates that actually contaminate the food supply, are the questions the team now hopes will drive the next round of research.

Subject of Research: Effects of long-term fungicide exposure on adaptation, antibiotic tolerance and virulence of the foodborne pathogen Bacillus cereus

Article Title: Long-term fungicide exposure promotes bacterial adaptation and increases virulence of foodborne pathogen Bacillus cereus in Caenorhabditis elegans

Article References: Wang, H.-Y., How, C. M., Li, Y.-S., Mao, Y., Nguyen, T. H., & Wei, C.-C. (2026). Long-term fungicide exposure promotes bacterial adaptation and increases virulence of foodborne pathogen Bacillus cereus in Caenorhabditis elegans. Current Research in Food Science, 13, Article 101572. https://doi.org/10.1016/j.crfs.2026.101572

Image Credits: AI Generated

DOI: 10.1016/j.crfs.2026.101572

Keywords: Bacillus cereus, fungicide exposure, antimicrobial tolerance, biofilm formation, Caenorhabditis elegans, tebuconazole, chlorothalonil, propineb, virulence genes, food safety, foodborne pathogen, efflux pumps

Benzo[a]pyrene, often abbreviated BaP, belongs to the polycyclic aromatic hydrocarbons, a family of compounds assembled from fused aromatic rings and generated mainly by the combustion of fossil fuels, plant biomass, and petroleum derivatives. These molecules are persistent, highly lipophilic, and notorious for their affinity for particulate surfaces. In aquatic organisms they are associated with narcosis, cardiac dysfunction, mutagenicity, and carcinogenicity, and BaP in particular ranks among the most potent genotoxic and bioaccumulative agents known in aquatic toxicology. Microplastics, meanwhile, have become so widespread that measuring their effects in isolation increasingly misses the point. Contaminants in rivers and lakes rarely arrive alone, and microplastic particles, with their vast hydrophobic surface areas, are prime candidates to interact chemically with hydrocarbons dissolved in the water.

The research team, led by Yuuri Gabriel de Souza Santos of Universidade Santa Cecília together with colleagues from Universidade Santa Cecília and the Universidade Federal de São Paulo, designed a full-factorial exposure experiment to disentangle these interactions. Cultures of Raphidocelis subcapitata were exposed for 72 hours under tightly controlled conditions of temperature, light, and agitation to low-density polyethylene microplastics at three concentrations: 5, 50, and 500 milligrams per liter. The lowest of these reflects concentrations actually reported in freshwater environments, while the higher doses were intended to simulate more extreme pollution scenarios. Each microplastic treatment was tested alone and in combination with the median effective concentration of BaP, the dose that inhibits algal growth by fifty percent, which the team first determined experimentally for this species.

That determination produced a sobering baseline. The calculated EC50 for BaP in R. subcapitata was approximately 21 micrograms per liter, with a 95 percent confidence interval of 20 to 25 micrograms per liter. Even the lowest concentration tested, 3 micrograms per liter, caused statistically significant growth inhibition, marking it as the lowest observed effect concentration under the study’s conditions. At the highest dose of 39 micrograms per liter, growth inhibition approached 90 percent. The estimated EC50 falls squarely within the range of BaP concentrations documented in contaminated freshwater systems worldwide, where water column values typically span from less than a hundredth of a microgram to roughly 2.4 micrograms per liter, and sediments can hold far higher burdens. In other words, the toxicological benchmark established in the laboratory is uncomfortably close to what polluted rivers actually deliver.

The mechanism behind BaP’s damage to algae is thought to involve both photosynthetic disruption and direct membrane interactions. As a lipophilic compound, BaP binds readily to the lipid bilayers of algal cells, and polycyclic aromatic hydrocarbons can drive excessive production of reactive oxygen species through interference with cellular electron transport. Prior work has also shown that high hydrocarbon loads impair chlorophyll production, starving cells of photosynthetic capacity. Intriguingly, during routine microscopic examination the researchers occasionally observed clumps of lipids forming on the outer surfaces of BaP-exposed cells, a response consistent with previous reports that green algae increase membrane lipids as a defensive strategy against cytotoxic hydrocarbon damage.

When the microplastics were tested on their own, the results defied simple dose-response logic. At 5 and 50 milligrams per liter, the polyethylene particles significantly reduced algal density, an effect the authors attribute largely to chemical additives incorporated into the polymer, such as plasticizers, antioxidants, UV stabilizers, lubricants, and pigments. Because these additives are not covalently bound to the plastic matrix, they can leach into the surrounding water and exert their own toxicity; benzotriazole UV stabilizers, for example, have previously been shown to harm the freshwater alga Chlamydomonas reinhardtii. Yet at 500 milligrams per liter, toxicity vanished entirely and algal biomass actually exceeded the control by 3.7 percent, surpassing the lower-dose treatments by more than 40 percent. The most plausible explanation is that the enormous particle surface area at high concentrations provided an ideal substrate for biofilm formation, effectively turning the plastic into a growth platform for the microorganisms it would otherwise harm.

The combined exposures produced the study’s most consequential findings. BaP alone at 21 micrograms per liter inhibited roughly 57.6 percent of algal growth. But when the same BaP concentration was paired with 50 or 500 milligrams per liter of microplastics, inhibition dropped sharply to about 34.9 and 22.8 percent respectively, both statistically distinct from BaP alone. The interpretation is that at these higher particle densities, the hydrophobic hydrocarbon preferentially sorbs onto plastic surfaces, sequestering it away from the water column and lowering its effective bioavailability to the algae. This protective sorption effect mirrors previous observations in gammarids, cladocerans, sea urchins, and mysids, and echoes a study of juvenile common gobies in which microplastics delayed pyrene-induced mortality from 48 to 60 hours. Plastic, in these scenarios, acts as a temporary chemical sponge.

At the environmentally relevant concentration, however, the picture reversed into genuine concern. When just 5 milligrams per liter of microplastics accompanied the BaP, inhibition remained essentially unchanged from BaP alone, at about 58.3 percent, and both treatments were significantly more toxic than controls. This dose of plastic was evidently too low to strip a meaningful fraction of BaP from solution, leaving the hydrocarbon free to attack cell membranes. Since 5 milligrams per liter reflects concentrations documented in real freshwater systems, the message for regulators is troubling: at realistic pollution levels, microplastics do nothing to buffer hydrocarbon toxicity, while the plastic itself independently inhibits growth at that same dose.

The authors emphasize that this is the first study to evaluate combined BaP and microplastic effects in Raphidocelis subcapitata, and that their generalized linear model analyses confirmed a statistically significant interaction between the two contaminants, meaning the impact of each depends on the level of the other. The relationship is explicitly nonlinear: microplastics can either enhance or mitigate BaP toxicity depending on their concentration, rendering simple additive assumptions obsolete. Fourier transform infrared spectroscopy confirmed the test particles were linear low-density polyethylene, the polymer characteristically identified by split methylene peaks and methyl-group bands in its spectrum, matching the manufacturer’s specification.

The ecological stakes extend well beyond a single algal species. As primary producers, freshwater microalgae drive oxygen production, nutrient cycling, and energy transfer through food webs, and both microplastics and hydrocarbons can bioaccumulate in algal cells before moving to higher trophic levels. Green algae such as R. subcapitata are also valued agents of PAH bioremediation, and the new results raise questions about whether plastic contamination could undermine that cleanup capacity by altering hydrocarbon bioavailability. The authors acknowledge limitations: BaP adsorption onto the particles was not directly quantified, and responses such as chlorophyll content, oxidative stress, and gene expression were not measured. Notably, prior work on marine invertebrates found that even when survival appeared unaffected by combined exposures, surviving organisms carried DNA damage and elevated lipid peroxidation, hinting that growth-based endpoints may understate harm. The team calls for future research on chronic effects, trophic transfer, and additional freshwater species under environmentally realistic conditions, and concludes that microplastics cannot be treated as inert particles in aquatic systems. Their concentration, not merely their presence, may determine whether they worsen or mask the toxicity of the organic pollutants they travel with.

Subject of Research: Interactive toxicity of low-density polyethylene microplastics and benzo[a]pyrene in the freshwater microalga Raphidocelis subcapitata

Article Title: Interactive effects of low-density polyethylene microplastics and benzo[a]pyrene on the growth of the freshwater microalgae Raphidocelis subcapitata

Article References: de Souza Santos, Y. G., Choueri, R. B., Nobre, C. R., Simões, F. R., & Gusso-Choueri, P. K. (2026). Interactive effects of low-density polyethylene microplastics and benzo[a]pyrene on the growth of the freshwater microalgae Raphidocelis subcapitata. Ecotoxicology, 35(7), Article 161. https://doi.org/10.1007/s10646-026-03143-3

Image Credits: AI Generated

DOI: 10.1007/s10646-026-03143-3

Keywords: microplastics, benzo[a]pyrene, Raphidocelis subcapitata, freshwater ecotoxicology, polycyclic aromatic hydrocarbons, low-density polyethylene, algal growth inhibition, bioavailability, sorption, additive leaching, biofilm formation, ecological risk assessment

SpoVG was first characterized decades ago in the spore-forming bacterium Bacillus subtilis, where it was linked to sporulation and to the regulation of capsular polysaccharide synthesis in Staphylococcus aureus. In Listeria, however, its functions had remained largely unexplored. The new work shows that the protein is far more than a vestige of its sporulation-related past. By constructing deletion mutants and comparing their behavior with that of wild-type bacteria across a battery of assays, the researchers found that loss of spoVG reshapes the organism’s surface properties, its capacity to adhere to abiotic surfaces, and the architecture of the biofilms it builds.

Biofilms are central to Listeria’s persistence in food-processing environments. Once a population anchors itself to a surface and encases itself in a self-produced matrix of extracellular DNA, proteins, and polysaccharides, it becomes dramatically more resistant to sanitizers and desiccation. The study demonstrates that SpoVG-deficient mutants form biofilms with altered biomass and structural organization, indicating that the regulator influences the developmental program that converts free-swimming cells into a sessile community. Because biofilm-resident cells are a well-documented source of recurring contamination in ready-to-eat food production, understanding the genetic switches that govern this transition has direct practical value.

The pleiotropic nature of SpoVG’s influence is what makes the result particularly striking. Transcript-level comparisons suggest that the protein affects the expression of genes involved in motility, stress tolerance, and cell-envelope maintenance in addition to biofilm-associated functions. This breadth of action is characteristic of global regulators, proteins that do not catalyze specific metabolic steps but instead rewire large transcriptional programs in response to environmental cues. For Listeria, which must toggle between soil, food, and the mammalian cytosol within a single life cycle, such master switches are essential for rapid physiological remodeling.

Multi-dimensional niche establishment, the phrase the authors use to describe the pathogen’s ecological flexibility, encompasses growth at refrigeration temperatures, tolerance of acidic and osmotic stress, survival on inert surfaces, and intracellular proliferation in host tissue. The experiments indicate that SpoVG contributes to several of these dimensions at once. Mutants lacking the regulator showed measurable differences in phenotypes associated with environmental persistence, reinforcing the idea that a single conserved factor helps integrate the disparate signals a Listeria cell encounters as it moves between niches.

Mechanistically, SpoVG belongs to a small family of bacterial RNA-binding proteins that can associate with specific mRNA targets and influence their stability or translation. Work in other Gram-positive organisms has shown that such proteins allow bacteria to fine-tune gene expression post-transcriptionally, a level of control that complements classical transcription-factor regulation. In Listeria, this post-transcriptional layer may be especially important during the transitions between life on a surface and life inside a host, when mRNA turnover needs to be rapid and coordinated across functional gene groups.

From an applied perspective, the study suggests that interfering with SpoVG function could weaken Listeria on multiple fronts simultaneously. A compound or intervention that disrupts the regulator’s activity would be expected not only to impair biofilm maturation, reducing surface persistence, but also to compromise the stress responses that allow the organism to endure cleaning regimes and cold-chain conditions. Because SpoVG is conserved among Listeria strains, targeting it may offer broad protection against the genetic diversity found in industrial environments, where different isolates can carry varied resistance profiles.

The findings also carry implications for risk-assessment modeling. Current predictive tools for Listeria growth and survival rely heavily on environmental parameters such as temperature, pH, and water activity, but they incorporate the underlying genetics only crudely. Identifying regulators like SpoVG that govern multi-trait persistence provides a mechanistic bridge between genotype and phenotype, potentially allowing modelers to distinguish high-risk strains that harbor robust regulatory capacity from those that do not. That, in turn, could sharpen the allocation of monitoring resources in food-production facilities.

As with any single-gene study in an organism as adaptable as Listeria, important questions remain. Which mRNA targets does SpoVG bind directly, and how does environmental signaling modulate that binding? How do its effects intersect with better-characterized transcriptional regulators such as PrfA, Sigma B, and MogR, which control virulence and stress programs? Answering these questions will require RNA-binding assays, comparative transcriptomics across conditions, and structural work on the protein itself. What the current study establishes, however, is that SpoVG deserves a place among the small set of factors that define how Listeria monocytogenes builds communities, withstands hostile conditions, and colonizes new environments, a profile that makes it a compelling candidate for next-generation control strategies in food safety.

Subject of Research: SpoVG regulation of biofilm formation and niche adaptation in Listeria monocytogenes

Article Title: SpoVG as a pleiotropic regulator modulating Listeria monocytogenes biofilm formation and multi-dimensional niche establishment

Article References: Shi, C., Zhu, P., Li, R., Chen, H., Meng, F., Lu, Z., & Bie, X. (2026). SpoVG as a pleiotropic regulator modulating Listeria monocytogenes biofilm formation and multi-dimensional niche establishment. npj Science of Food. https://doi.org/10.1038/s41538-026-01134-6

Image Credits: AI Generated

DOI: 10.1038/s41538-026-01134-6

Keywords: Listeria monocytogenes, SpoVG, biofilm formation, food safety, gene regulation, RNA-binding protein, pleiotropic regulator, foodborne pathogen, environmental persistence, bacterial stress response, npj Science of Food, microbiology