# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 56 | 0 | 0.9906 | Protein phosphatase AP2C1 negatively regulates basal resistance and defense responses to Pseudomonas syringae. Mitogen-activated protein kinases (MAPKs) mediate plant immune responses to pathogenic bacteria. However, less is known about the cell autonomous negative regulatory mechanism controlling basal plant immunity. We report the biological role of Arabidopsis thaliana MAPK phosphatase AP2C1 as a negative regulator of plant basal resistance and defense responses to Pseudomonas syringae. AP2C2, a closely related MAPK phosphatase, also negatively controls plant resistance. Loss of AP2C1 leads to enhanced pathogen-induced MAPK activities, increased callose deposition in response to pathogen-associated molecular patterns or to P. syringae pv. tomato (Pto) DC3000, and enhanced resistance to bacterial infection with Pto. We also reveal the impact of AP2C1 on the global transcriptional reprogramming of transcription factors during Pto infection. Importantly, ap2c1 plants show salicylic acid-independent transcriptional reprogramming of several defense genes and enhanced ethylene production in response to Pto. This study pinpoints the specificity of MAPK regulation by the different MAPK phosphatases AP2C1 and MKP1, which control the same MAPK substrates, nevertheless leading to different downstream events. We suggest that precise and specific control of defined MAPKs by MAPK phosphatases during plant challenge with pathogenic bacteria can strongly influence plant resistance. | 2017 | 28062592 |
| 7887 | 1 | 0.9904 | Double-edged sword effects of sulfate reduction process in sulfur autotrophic denitrification system: Accelerating nitrogen removal and promoting antibiotic resistance genes spread. This study proposed the double-edged sword effects of sulfate reduction process on nitrogen removal and antibiotic resistance genes (ARGs) transmission in sulfur autotrophic denitrification system. Excitation-emission matrix-parallel factor analysis identified the protein-like fraction in soluble microbial products as main endogenous organic matter driving the sulfate reduction process. The resultant sulfide tended to serve as bacterial modulators, augmenting electron transfer processes and mitigating oxidative stress, thereby enhancing sulfur oxidizing bacteria (SOB) activity, rather than extra electron donors. The cooperation between SOB and heterotroph (sulfate reducing bacteria (SRB) and heterotrophic denitrification bacteria (HDB)) were responsible for advanced nitrogen removal, facilitated by multiple metabolic pathways including denitrification, sulfur oxidation, and sulfate reduction. However, SRB and HDB were potential ARGs hosts and assimilatory sulfate reduction pathway positively contributed to ARGs spread. Overall, the sulfate reduction process in sulfur autotrophic denitrification system boosted nitrogen removal process, but also increased the risk of ARGs transmission. | 2024 | 39122125 |
| 590 | 2 | 0.9900 | Recent advances in functional assays of WRKY transcription factors in plant immunity against pathogens. WRKY transcription factors (TFs) are one of the largest transcription factor families in plants and play important roles in plant processes, most notably in responding to diverse biotic and abiotic stresses. This article reviews the recent research progresses on WRKY TFs in regulating plant immunity, which includes both positive and negative regulation. WRKY TFs were shown to regulate plant defense against pathogens including fungi, bacteria, oomycetes, and viruses by modulating downstream pathogen resistance genes or interacting with other regulators. Plant signaling pathways or components involved in the regulatory network of WRKY-mediated plant immunity mainly involve the action of phytohormones, MAPKs (Mitogen-activated protein kinases), and other transcription factors. The interaction of WRKY TFs with these factors during pathogen resistance was discussed in this article, which may contribute to understanding the mechanisms of WRKY transcription factors in plant immunity. | 2024 | 39917597 |
| 8614 | 3 | 0.9898 | Polystyrene nanoparticles induce biofilm formation in Pseudomonas aeruginosa. In recent years, micro/nanoplastics have garnered widespread attention due to their ecological risks. In this study, we investigated the effects of polystyrene nanoparticles (PS-NPs) of different sizes on the growth and biofilm formation of Pseudomonas aeruginosa PAO1. The results demonstrated that exposure to certain concentrations of PS-NPs significantly promoted bacterial biofilm formation. Meanwhile, we comprehensively revealed its mechanism whereby PS-NPs induced oxidative stress and altered bacterial membrane permeability by contacting or penetrating bacterial membranes. To counteract the stimulation by PS-NPs and reduce their toxicity, bacteria enhanced biofilm formation by upregulating the expression of biofilm-related genes, increasing EPS and virulence factors secretion, and enhancing bacterial motility through the participation of the quorum sensing (QS) system. Additionally, we also found that exposure to PS-NPs enhanced bacterial antibiotic resistance, posing a challenge to antimicrobial therapy. Our study reveals the toxic effects of nanoplastics and the defense mechanisms of bacteria, which has important implications for the risk assessment and management of environmental nanoplastics. | 2024 | 38442601 |
| 8487 | 4 | 0.9897 | Mechanisms of nano zero-valent iron in enhancing dibenzofuran degradation by a Rhodococcus sp.: Trade-offs between ATP production and protection against reactive oxygen species. Nano zero-valent iron (nZVI) can enhance pollutants biodegradation, but it displays toxicity towards microorganisms. Gram-positive (G(+)) bacteria exhibit greater resistance to nZVI than Gram-negative bacteria. However, mechanisms of nZVI accelerating pollutants degradation by G(+) bacteria remain unclear. Herein, we explored effects of nZVI on a G(+) bacterium, Rhodococcus sp. strain p52, and mechanisms by which nZVI accelerates biodegradation of dibenzofuran, a typical polycyclic aromatic compound. Electron microscopy and energy dispersive spectroscopy analysis revealed that nZVI could penetrate cell membranes, which caused damage and growth inhibition. nZVI promoted dibenzofuran biodegradation at certain concentrations, while higher concentration functioned later due to the delayed reactive oxygen species (ROS) mitigation. Transcriptomic analysis revealed that cells adopted response mechanisms to handle the elevated ROS induced by nZVI. ATP production was enhanced by accelerated dibenzofuran degradation, providing energy for protein synthesis related to antioxidant stress and damage repair. Meanwhile, electron transport chain (ETC) was adjusted to mitigate ROS accumulation, which involved downregulating expression of ETC complex I-related genes, as well as upregulating expression of the genes for the ROS-scavenging cytochrome bd complex and ETC complex II. These findings revealed the mechanisms underlying nZVI-enhanced biodegradation by G(+) bacteria, offering insights into optimizing bioremediation strategies involving nZVI. | 2025 | 39549579 |
| 8150 | 5 | 0.9897 | ROS production during symbiotic infection suppresses pathogenesis-related gene expression. Leguminous plants have exclusive ability to form symbiotic relationship with soil bacteria of the genus Rhizobium. Symbiosis is a complex process that involves multiple molecular signaling activities, such as calcium fluxes, production of reactive oxygen species (ROS) and synthesis of nodulation genes. We analyzed the role of ROS in defense gene expression in Medicago truncatula during symbiosis and pathogenesis. Studies in Arabidopsis thaliana showed that the induction of pathogenesis-related (PR) genes during systemic acquired resistance (SAR) is regulated by NPR1 protein, which resides in the cytoplasm as an oligomer. After oxidative burst and return of reducing conditions, the NPR1 undergoes monomerization and becomes translocated to the nucleus, where it functions in PR genes induction. We show that ROS production is both stronger and longer during symbiotic interactions than during interactions with pathogenic, nonhost or common nonpathogenic soil bacteria. Moreover, root cells inoculated with Sinorhizobium meliloti accumulated ROS in the cytosol but not in vacuoles, as opposed to Pseudomonas putida inoculation or salt stress treatment. Furthermore, increased ROS accumulation by addition of H₂O₂ reduced the PR gene expression, while catalase had an opposite effect, establishing that the PR gene expression is opposite to the level of cytoplasmic ROS. In addition, we show that salicylic acid pretreatment significantly reduced ROS production in root cells during symbiotic interaction. | 2012 | 22499208 |
| 8766 | 6 | 0.9897 | Partitioning the Effects of Soil Legacy and Pathogen Exposure Determining Soil Suppressiveness via Induced Systemic Resistance. Beneficial host-associated bacteria can assist plant protection against pathogens. In particular, specific microbes are able to induce plant systemic resistance. However, it remains largely elusive which specific microbial taxa and functions trigger plant immune responses associated with disease suppression. Here, we experimentally studied this by setting up two independent microcosm experiments that differed in the time at which plants were exposed to the pathogen and the soil legacy (i.e., soils with historically suppressive or conducive). Overall, we found soil legacy effects to have a major influence on disease suppression irrespective of the time prior to pathogen exposure. Rhizosphere bacterial communities of tomato plants were significantly different between the two soils, with potential beneficial strains occurring at higher relative abundances in the suppressive soil. Root transcriptome analysis revealed the soil legacy to induce differences in gene expression, most importantly, genes involved in the pathway of phenylpropanoid biosynthesis. Last, we found genes in the phenylpropanoid biosynthesis pathway to correlate with specific microbial taxa, including Gp6, Actinomarinicola, Niastella, Phaeodactylibacter, Longimicrobium, Bythopirellula, Brevundimonas, Ferruginivarius, Kushneria, Methylomarinovum, Pseudolabrys, Sphingobium, Sphingomonas, and Alterococcus. Taken together, our study points to the potential regulation of plant systemic resistance by specific microbial taxa, and the importance of soil legacy on disease incidence and eliciting plant-defense mechanisms. | 2022 | 36365269 |
| 20 | 7 | 0.9897 | Paraburkholderia phytofirmans PsJN triggers local and systemic transcriptional reprogramming in Arabidopsis thaliana and increases resistance against Botrytis cinerea. Fungal pathogens are one of the main causes of yield losses in many crops, severely affecting agricultural production worldwide. Among the various approaches to alleviate this problem, beneficial microorganisms emerge as an environmentally friendly and sustainable alternative. In addition to direct biocontrol action against pathogens, certain plant growth-promoting bacteria (PGPB) enhance the plant immune defense to control diseases through induced systemic resistance (ISR). Paraburkholderia phytofirmans PsJN has been shown as an efficient biocontrol agent against diseases. However, the specific mechanisms underlying these beneficial effects at both local and systemic level remain largely unknown. In this study, we investigated the transcriptional response of Arabidopsis thaliana at above- and below-ground levels upon interaction with P. phytofirmans PsJN, and after Botrytis cinerea infection. Our data clearly support the protective effect of P. phytofirmans PsJN through ISR against B. cinerea in plants grown in both soil and hydroponic conditions. The comparative transcriptome analysis of the mRNA and miRNA sequences revealed that PsJN modulates the expression of genes involved in abiotic stress responses, microbe-plant interactions and ISR, with ethylene signaling pathway genes standing out. In roots, PsJN predominantly downregulated the expression of genes related to microbe perception, signaling and immune response, indicating that PsJN locally provoked attenuation of defense responses to facilitate and support colonization and the maintenance of mutualistic relationship. In leaves, the increased expression of defense-related genes prior to infection in combination with the protective effect of PsJN observed in later stages of infection suggests that bacterial inoculation primes plants for enhanced systemic immune response after subsequent pathogen attack. | 2025 | 40530279 |
| 8609 | 8 | 0.9896 | Nano-biochar regulates phage-host interactions, reducing antibiotic resistance genes in vermicomposting systems. Biochar amendment reshapes microbial community dynamics in vermicomposting, but the mechanism of how phages respond to this anthropogenic intervention and regulate the dissemination of antibiotic resistance genes (ARGs) remains unclear. In this study, we used metagenomics, viromics, and laboratory validation to explore how nano-biochar affects phage-host interactions and ARGs dissemination in vermicomposting. Our results revealed distinct niche-specific phage life strategies. In vermicompost, lytic phages dominated and used a "kill-the-winner" strategy to suppress antibiotic-resistant bacteria (ARB). In contrast, lysogenic phages prevailed in the earthworm gut, adopting a "piggyback-the-winner" strategy that promoted ARGs transduction through mutualistic host interactions. Nano-biochar induced the conversion of lysogenic to lytic phages in the earthworm gut, while concurrently reducing the abundance of lysogenic phages and their encoded auxiliary metabolic genes carried by ARB. This shift disrupted phage-host mutualism and inhibited ARGs transmission via a "phage shunting" mechanism. In vitro validation with batch culture experiments further confirmed that lysogenic phages increased transduction of ARGs in the earthworm gut, while nano-biochar reduced the spread of ARGs by enhancing lysis infectivity. Our study constructs a mechanistic framework linking nano-biochar induced shifts in phage lifestyles that suppress ARG spread, offering insights into phage-host coadaptation and resistance mitigation strategies in organic waste treatment ecosystems. | 2025 | 40838886 |
| 589 | 9 | 0.9895 | Insulin Signaling and Insulin Resistance Facilitate Trained Immunity in Macrophages Through Metabolic and Epigenetic Changes. Adaptation of the innate immune system has been recently acknowledged, explaining sustained changes of innate immune responses. Such adaptation is termed trained immunity. Trained immunity is initiated by extracellular signals that trigger a cascade of events affecting cell metabolism and mediating chromatin changes on genes that control innate immune responses. Factors demonstrated to facilitate trained immunity are pathogenic signals (fungi, bacteria, viruses) as well non-pathogenic signals such as insulin, cytokines, adipokines or hormones. These signals initiate intracellular signaling cascades that include AKT kinases and mTOR as well as histone methylases and demethylases, resulting in metabolic changes and histone modifications. In the context of insulin resistance, AKT signaling is affected resulting in sustained activation of mTORC1 and enhanced glycolysis. In macrophages elevated glycolysis readily impacts responses to pathogens (bacteria, fungi) or danger signals (TLR-driven signals of tissue damage), partly explaining insulin resistance-related pathologies. Thus, macrophages lacking insulin signaling exhibit reduced responses to pathogens and altered metabolism, suggesting that insulin resistance is a state of trained immunity. Evidence from Insulin Receptor as well as IGF1Receptor deficient macrophages support the contribution of insulin signaling in macrophage responses. In addition, clinical evidence highlights altered macrophage responses to pathogens or metabolic products in patients with systemic insulin resistance, being in concert with cell culture and animal model studies. Herein, we review the current knowledge that supports the impact of insulin signaling and other insulin resistance related signals as modulators of trained immunity. | 2019 | 31244863 |
| 8616 | 10 | 0.9895 | Mechanisms of inhibition and recovery under multi-antibiotic stress in anammox: A critical review. With the escalating global concern for emerging pollutants, particularly antibiotics, microplastics, and nanomaterials, the potential disruption they pose to critical environmental processes like anaerobic ammonia oxidation (anammox) has become a pressing issue. The anammox process, which plays a crucial role in nitrogen removal from wastewater, is particularly sensitive to external pollutants. This paper endeavors to address this knowledge gap by providing a comprehensive overview of the inhibition mechanisms of multi-antibiotic on anaerobic ammonia-oxidizing bacteria, along with insights into their recovery processes. The paper dives deeply into the various ways antibiotics interact with anammox bacteria, focusing specifically on their interference with the bacteria's extracellular polymers (EPS) - crucial components that maintain the structural integrity and functionality of the cells. Additionally, it explores how anammox bacteria utilize quorum sensing (QS) mechanisms to regulate their community structure and respond to antibiotic stress. Moreover, the paper summarizes effective removal methods for these antibiotics from wastewater systems, which is crucial for mitigating their inhibitory effects on anammox bacteria. Finally, the paper offers valuable insights into how anammox communities can recuperate from multi-antibiotic stress. This includes strategies for reintroducing healthy bacteria, optimizing operational conditions, and using bioaugmentation techniques to enhance the resilience of anammox communities. In summary, this paper not only enriches our understanding of the complex interactions between antibiotics and anammox bacteria but also provides theoretical and practical guidance for the treatment of antibiotic pollution in sewage, ensuring the sustainability and effectiveness of wastewater treatment processes. | 2024 | 39366232 |
| 24 | 11 | 0.9895 | Environmental History Modulates Arabidopsis Pattern-Triggered Immunity in a HISTONE ACETYLTRANSFERASE1-Dependent Manner. In nature, plants are exposed to a fluctuating environment, and individuals exposed to contrasting environmental factors develop different environmental histories. Whether different environmental histories alter plant responses to a current stress remains elusive. Here, we show that environmental history modulates the plant response to microbial pathogens. Arabidopsis thaliana plants exposed to repetitive heat, cold, or salt stress were more resistant to virulent bacteria than Arabidopsis grown in a more stable environment. By contrast, long-term exposure to heat, cold, or exposure to high concentrations of NaCl did not provide enhanced protection against bacteria. Enhanced resistance occurred with priming of Arabidopsis pattern-triggered immunity (PTI)-responsive genes and the potentiation of PTI-mediated callose deposition. In repetitively stress-challenged Arabidopsis, PTI-responsive genes showed enrichment for epigenetic marks associated with transcriptional activation. Upon bacterial infection, enrichment of RNA polymerase II at primed PTI marker genes was observed in environmentally challenged Arabidopsis. Finally, repetitively stress-challenged histone acetyltransferase1-1 (hac1-1) mutants failed to demonstrate enhanced resistance to bacteria, priming of PTI, and increased open chromatin states. These findings reveal that environmental history shapes the plant response to bacteria through the development of a HAC1-dependent epigenetic mark characteristic of a primed PTI response, demonstrating a mechanistic link between the primed state in plants and epigenetics. | 2014 | 24963055 |
| 736 | 12 | 0.9895 | Resistance Is Not Futile: The Role of Quorum Sensing Plasticity in Pseudomonas aeruginosa Infections and Its Link to Intrinsic Mechanisms of Antibiotic Resistance. Bacteria use a cell-cell communication process called quorum sensing (QS) to orchestrate collective behaviors. QS relies on the group-wide detection of extracellular signal molecules called autoinducers (AI). Quorum sensing is required for virulence and biofilm formation in the human pathogen Pseudomonas aeruginosa. In P. aeruginosa, LasR and RhlR are homologous LuxR-type soluble transcription factor receptors that bind their cognate AIs and activate the expression of genes encoding functions required for virulence and biofilm formation. While some bacterial signal transduction pathways follow a linear circuit, as phosphoryl groups are passed from one carrier protein to another ultimately resulting in up- or down-regulation of target genes, the QS system in P. aeruginosa is a dense network of receptors and regulators with interconnecting regulatory systems and outputs. Once activated, it is not understood how LasR and RhlR establish their signaling hierarchy, nor is it clear how these pathway connections are regulated, resulting in chronic infection. Here, we reviewed the mechanisms of QS progression as it relates to bacterial pathogenesis and antimicrobial resistance and tolerance. | 2022 | 35744765 |
| 7926 | 13 | 0.9894 | Microplastics Exacerbated Conjugative Transfer of Antibiotic Resistance Genes during Ultraviolet Disinfection: Highlighting Difference between Conventional and Biodegradable Ones. Microplastics (MPs) have been confirmed as a hotspot for antibiotic resistance genes (ARGs) in wastewater. However, the impact of MPs on the transfer of ARGs in wastewater treatment remains unclear. This study investigated the roles and mechanisms of conventional (polystyrene, PS) and biodegradable (polylactic acid, PLA) MPs in the conjugative transfer of ARGs during ultraviolet disinfection. The results showed that MPs significantly facilitated the conjugative transfer of ARGs compared with individual ultraviolet disinfection, and PSMPs exhibited higher facilitation than PLAMPs. The facilitation effects were attributed to light shielding and the production of reactive oxygen species (ROS) and nanoplastics from ultraviolet irradiation of MPs. The light shielding of MPs protected the bacteria and ARGs from ultraviolet inactivation. More importantly, ROS and nanoplastics generated from irradiated MPs induced intracellular oxidative stress on bacteria and further increased the cell membrane permeability and intercellular contact, ultimately enhancing the ARG exchange. The greater fragmentation of PSMPs than PLAMPs resulted in a higher intracellular oxidative stress and a stronger enhancement. This study highlights the concerns of conventional and biodegradable MPs associated with the transfer of ARGs during wastewater treatment, which provides new insights into the combined risks of MPs and ARGs in the environment. | 2025 | 39723446 |
| 8329 | 14 | 0.9894 | Protozoan predation enhances stress resistance and antibiotic tolerance in Burkholderia cenocepacia by triggering the SOS response. Bacterivorous protists are thought to serve as training grounds for bacterial pathogens by subjecting them to the same hostile conditions that they will encounter in the human host. Bacteria that survive intracellular digestion exhibit enhanced virulence and stress resistance after successful passage through protozoa but the underlying mechanisms are unknown. Here we show that the opportunistic pathogen Burkholderia cenocepacia survives phagocytosis by ciliates found in domestic and hospital sink drains, and viable bacteria are expelled packaged in respirable membrane vesicles with enhanced resistance to oxidative stress, desiccation, and antibiotics, thereby contributing to pathogen dissemination in the environment. Reactive oxygen species generated within the protozoan phagosome promote the formation of persisters tolerant to ciprofloxacin by activating the bacterial SOS response. In addition, we show that genes encoding antioxidant enzymes are upregulated during passage through ciliates increasing bacterial resistance to oxidative radicals. We prove that suppression of the SOS response impairs bacterial intracellular survival and persister formation within protists. This study highlights the significance of protozoan food vacuoles as niches that foster bacterial adaptation in natural and built environments and suggests that persister switch within phagosomes may be a widespread phenomenon in bacteria surviving intracellular digestion. | 2024 | 38366016 |
| 55 | 15 | 0.9893 | Effector-triggered and pathogen-associated molecular pattern-triggered immunity differentially contribute to basal resistance to Pseudomonas syringae. Pathogens induce pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) in plants. PAMPs are microbial molecules recognized by host plants as nonself signals, whereas pathogen effectors are evolved to aid in parasitism but are sometimes recognized by specific intracellular resistance proteins. In the absence of detectable ETI determining classical incompatible interactions, basal resistance exists during compatible and nonhost interactions. What triggers the basal resistance has remained elusive. Here, we provide evidence that ETI contributes to basal resistance during both compatible and nonhost Arabidopsis-Pseudomonas syringae interactions. Mutations in RAR1 and NDR1, two genes required for ETI, compromise basal resistance in both compatible and nonhost interactions. Complete nonhost resistance to P. syringae pv. tabaci required a functional type III secretion system. PTI appears to play a greater role in nonhost resistance than basal resistance during compatible interactions, because abrogation of PTI compromises basal resistance during nonhost but not compatible interactions. Strikingly, simultaneous abrogation of ETI and flagellin-induced PTI rendered plants completely susceptible to the nonadapted bacterium P. syringae pv. tabaci, indicating that ETI and PTI act synergistically during nonhost resistance. Thus, both nonhost resistance and basal resistance to virulent bacteria can be unified under PTI and ETI. | 2010 | 20521956 |
| 8144 | 16 | 0.9893 | Fungal Priming: Prepare or Perish. Priming (also referred to as acclimation, acquired stress resistance, adaptive response, or cross-protection) is defined as an exposure of an organism to mild stress that leads to the development of a subsequent stronger and more protective response. This memory of a previously encountered stress likely provides a strong survival advantage in a rapidly shifting environment. Priming has been identified in animals, plants, fungi, and bacteria. Examples include innate immune priming and transgenerational epigenetic inheritance in animals and biotic and abiotic stress priming in plants, fungi, and bacteria. Priming mechanisms are diverse and include alterations in the levels of specific mRNAs, proteins, metabolites, and epigenetic changes such as DNA methylation and histone acetylation of target genes. | 2022 | 35628704 |
| 8615 | 17 | 0.9893 | How anammox responds to the emerging contaminants: Status and mechanisms. Numerous researches have been carried out to study the effects of emerging contaminants in wastewater, such as antibiotics, nanomaterials, heavy metals, and microplastics, on the anammox process. However, they are fragmented and difficult to provide a comprehensive understanding of their effects on reactor performance and the metabolic mechanisms in anammox bacteria. Therefore, this paper overviews the effects on anammox processes by the introduced emerging contaminants in the past years to fulfill such knowledge gaps that affect our perception of the inhibitory mechanisms and limit the optimization of the anammox process. In detail, their effects on anammox processes from the aspects of reactor performance, microbial community, antibiotic resistance genes (ARGs), and functional genes related to anammox and nitrogen transformation in anammox consortia are summarized. Furthermore, the metabolic mechanisms causing the cell death of anammox bacteria, such as induction of reactive oxygen species, limitation of substrates diffusion, and membrane binding are proposed. By offering this review, the remaining research gaps are identified, and the potential metabolic mechanisms in anammox consortia are highlighted. | 2021 | 34087646 |
| 8489 | 18 | 0.9893 | Signaling molecules accelerate the transmission of antibiotic resistance genes under the stress of copper. Heavy metals can accelerate the dissemination of antibiotic resistance genes (ARGs) in aquatic environments by imposing environmental stresses. Signaling molecules play a role in bacterial communication and help bacteria adapt to environmental stresses. However, little is known whether the presence of signaling molecules has an effect on the spread of ARGs induced by heavy metals. In this study, we investigated how N-decanoyl-L-homoserine lactone (C10-HSL) affects copper-induced conjugative transfer of ARGs. We calculated the conjugative transfer frequency and measured reactive oxygen species (ROS) production, membrane permeability, and the expression of relevant genes. The results demonstrated that the addition of C10-HSL increased the conjugative transfer frequency of ARGs under copper ions (Cu(2+)) stress, showing a 7.2-fold increase under 0.5 μM Cu(2+) and 0.39 μM C10-HSL treatment compared to the control. This enhancement was associated with elevated intracellular ROS production and increased membrane permeability. The reduced conjugative transfer frequency under anaerobic conditions or with thiourea treatment supported the key role of ROS in this process. Furthermore, ROS overproduction triggered the SOS response, as evidenced by a 9-fold upregulation of recA expression. C10-HSL also modulated membrane-associated gene expression by upregulating outer membrane porins and downregulating efflux pump genes under Cu(2+)stress. This study provides a new insight into the spread of ARGs in aquatic environments. | 2025 | 40840413 |
| 8658 | 19 | 0.9892 | Microplastic exposure reshapes the virome and virus-bacteria networks with implications for immune regulation in Mytilus coruscus. Microplastic pollution has emerged as a critical environmental concern, yet its impacts on host-associated viral communities and immune balance in marine bivalves remain largely unexplored. In this study, Mytilus coruscus individuals were exposed to microplastics in situ for seven days. Virome sequencing and bioinformatic analyses revealed that microplastic exposure induced divergent responses in DNA and RNA viral communities. DNA viromes exhibited suppressed diversity and downregulation of core viral metabolic pathways, potentially reflecting reduced viral replication capacity under host immune stress. In contrast, RNA viromes displayed metabolic activation and functional shifts, including enriched glycan and nucleotide metabolism, possibly linked to enhanced viral activity or immune evasion. Phage-bacteria interaction networks were also restructured, showing increased associations with opportunistic pathogens such as Vibrio cholerae and Enterobacter, potentially affecting immune surveillance. Furthermore, the expression of antibiotic resistance genes (ARGs) in viral genomes was differentially regulated, suggesting pollutant-induced microbial selection that may challenge host immune resilience. These findings suggest that microplastics not only reshape virome composition and metabolic functions but also influence virus-mediated immune interactions, with important implications for disease susceptibility and immune homeostasis in filter-feeding shellfish. | 2025 | 41056669 |