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840000.9946Transferring knowledge of bacterial protein interaction networks to predict pathogen targeted human genes and immune signaling pathways: a case study on M. tuberculosis. BACKGROUND: Bacterial invasive infection and host immune response is fundamental to the understanding of pathogen pathogenesis and the discovery of effective therapeutic drugs. However, there are very few experimental studies on the signaling cross-talks between bacteria and human host to date. METHODS: In this work, taking M. tuberculosis H37Rv (MTB) that is co-evolving with its human host as an example, we propose a general computational framework that exploits the known bacterial pathogen protein interaction networks in STRING database to predict pathogen-host protein interactions and their signaling cross-talks. In this framework, significant interlogs are derived from the known pathogen protein interaction networks to train a predictive l(2)-regularized logistic regression model. RESULTS: The computational results show that the proposed method achieves excellent performance of cross validation as well as low predicted positive rates on the less significant interlogs and non-interlogs, indicating a low risk of false discovery. We further conduct gene ontology (GO) and pathway enrichment analyses of the predicted pathogen-host protein interaction networks, which potentially provides insights into the machinery that M. tuberculosis H37Rv targets human genes and signaling pathways. In addition, we analyse the pathogen-host protein interactions related to drug resistance, inhibition of which potentially provides an alternative solution to M. tuberculosis H37Rv drug resistance. CONCLUSIONS: The proposed machine learning framework has been verified effective for predicting bacteria-host protein interactions via known bacterial protein interaction networks. For a vast majority of bacterial pathogens that lacks experimental studies of bacteria-host protein interactions, this framework is supposed to achieve a general-purpose applicability. The predicted protein interaction networks between M. tuberculosis H37Rv and Homo sapiens, provided in the Additional files, promise to gain applications in the two fields: (1) providing an alternative solution to drug resistance; (2) revealing the patterns that M. tuberculosis H37Rv genes target human immune signaling pathways.201829954330
843610.9946NIR-Activated Hydrogel with Dual-Enhanced Antibiotic Effectiveness for Thorough Elimination of Antibiotic-Resistant Bacteria. Antibiotic resistance has become a critical health crisis globally. Traditional strategies using antibiotics can lead to drug-resistance, while inorganic antimicrobial agents can cause severe systemic toxicity. Here, we have developed a dual-antibiotic hydrogel delivery system (PDA-Ag@Levo/CMCS), which can achieve controlled release of clinical antibiotics levofloxacin (Levo) and classic nanoscale antibiotic silver nanoparticles (AgNPs), effectively eliminating drug-resistant P. aeruginosa. Benefiting from the photothermal (PTT) effect of polydopamine (PDA), the local high temperature generated by PDA-Ag@Levo/CMCS can quickly kill bacteria through continuous and responsive release of dual-antibiotics to restore sensitivity to ineffective antibiotics. Moreover, AgNPs could significantly improve the efficiency of traditional antibiotics by disrupting bacterial membranes and reducing their toxicity to healthy tissues. A clever combination of PTT and drug-combination therapy can effectively eliminate biofilms and drug-resistant bacteria. Mechanism studies have shown that PDA-Ag@Levo might eliminate drug-resistant P. aeruginosa by disrupting biofilm formation and protein synthesis, and inhibit the resistance mutation of P. aeruginosa by promoting the expression of related genes, such as rpoS, dinB, and mutS. Collectively, the synergistic effect of this dual-antibiotic hydrogel combined with PTT provides a creative strategy for eliminating drug-resistant bacteria in chronic infection wounds.202539760335
881820.9946Metatranscriptomic analysis of adaptive response of anammox bacteria Candidatus 'Kuenenia stuttgartiensis' to Zn(II) exposure. Zn(II) is frequently detected in biological nitrogen removal systems treating high-strength wastewater (e.g., landfill leachate), yet the cellular defense strategies of anammox bacteria against Zn(II) cytotoxicity is largely unknown. To uncover survival mechanisms under Zn(II) stress, responses of enriched anammox bacteria Candidatus 'Kuenenia stuttgartiensis' under exposure of various levels of Zn (II) were investigated through metatranscriptomic sequencing. Although increasing Zn(II) levels (50, 100 and 150 mg/L) resulted in decreasing anammox activities (86.1 ± 0.8%, 66.1 ± 1.4% and 43.9 ± 1.5% of the control, respectively), the viable cells in anammox sludge remained stable. Candidatus 'K. stuttgartiensis' possesses a complex network of regulatory systems to confer cells with the ability against Zn(II) toxicity, including functions related to substrate degradation, Zn(II) efflux, chelation, DNA repair, protein degradation, protein synthesis and signal transduction processes. Particularly, in order to maintain Zn(II) homeostasis, Candidatus 'K. stuttgartiensis' upregulated genes encoding RND efflux family (czcA, czcB, czcC, kustd1923 and kuste2279) for exporting Zn(II) actively. These heavy metal exporting genes could act as "sentinel genes" to detect the initial stage of Zn(II) inhibition on anammox bacteria, which might be beneficial to develop a diagnostic approach to predict the risk of operational failure when Zn(II) shock occurs.202031901527
829730.9946Novel RpoS-Dependent Mechanisms Strengthen the Envelope Permeability Barrier during Stationary Phase. Gram-negative bacteria have effective methods of excluding toxic compounds, including a largely impermeable outer membrane (OM) and a range of efflux pumps. Furthermore, when cells become nutrient limited, RpoS enacts a global expression change providing cross-protection against many stresses. Here, we utilized sensitivity to an anionic detergent (sodium dodecyl sulfate [SDS]) to probe changes occurring to the cell's permeability barrier during nutrient limitation. Escherichia coli is resistant to SDS whether cells are actively growing, carbon limited, or nitrogen limited. In actively growing cells, this resistance depends on the AcrAB-TolC efflux pump; however, this pump is not necessary for protection under either carbon-limiting or nitrogen-limiting conditions, suggesting an alternative mechanism(s) of SDS resistance. In carbon-limited cells, RpoS-dependent pathways lessen the permeability of the OM, preventing the necessity for efflux. In nitrogen-limited but not carbon-limited cells, the loss of rpoS can be completely compensated for by the AcrAB-TolC efflux pump. We suggest that this difference simply reflects the fact that nitrogen-limited cells have access to a metabolizable energy (carbon) source that can efficiently power the efflux pump. Using a transposon mutant pool sequencing (Tn-Seq) approach, we identified three genes, sanA, dacA, and yhdP, that are necessary for RpoS-dependent SDS resistance in carbon-limited stationary phase. Using genetic analysis, we determined that these genes are involved in two different envelope-strengthening pathways. These genes have not previously been implicated in stationary-phase stress responses. A third novel RpoS-dependent pathway appears to strengthen the cell's permeability barrier in nitrogen-limited cells. Thus, though cells remain phenotypically SDS resistant, SDS resistance mechanisms differ significantly between growth states. IMPORTANCE: Gram-negative bacteria are intrinsically resistant to detergents and many antibiotics due to synergistic activities of a strong outer membrane (OM) permeability barrier and efflux pumps that capture and expel toxic molecules eluding the barrier. When the bacteria are depleted of an essential nutrient, a program of gene expression providing cross-protection against many stresses is induced. Whether this program alters the OM to further strengthen the barrier is unknown. Here, we identify novel pathways dependent on the master regulator of stationary phase that further strengthen the OM permeability barrier during nutrient limitation, circumventing the need for efflux pumps. Decreased permeability of nutrient-limited cells to toxic compounds has important implications for designing new antibiotics capable of targeting Gram-negative bacteria that may be in a growth-limited state.201727821607
834840.9946Role of RelA-synthesized (p)ppGpp and ROS-induced mutagenesis in de novo acquisition of antibiotic resistance in E. coli. The stringent response of bacteria to starvation and stress also fulfills a role in addressing the threat of antibiotics. Within this stringent response, (p)ppGpp, synthesized by RelA or SpoT, functions as a global alarmone. However, the effect of this (p)ppGpp on resistance development is poorly understood. Here, we show that knockout of relA or rpoS curtails resistance development against bactericidal antibiotics. The emergence of mutated genes associated with starvation and (p)ppGpp, among others, indicates the activation of stringent responses. The growth rate is decreased in ΔrelA-resistant strains due to the reduced ability to synthesize (p)ppGpp and the persistence of deacylated tRNA impeding protein synthesis. Sluggish cellular activity causes decreased production of reactive oxygen species (ROS), thereby reducing oxidative damage, leading to weakened DNA mismatch repair, potentially reducing the generation of mutations. These findings offer new targets for mitigating antibiotic resistance development, potentially achieved through inhibiting (p)ppGpp or ROS synthesis.202438617560
848750.9946Mechanisms 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.202539549579
897860.9945Revealing the antibacterial power of hydrogen-releasing PdH nanohydride against drug resistant Staphylococcus aureus: an in-depth mechanism study. Currently, multidrug resistant (MDR) bacterial infections are a great threat to public health, and the development of novel strategies for high efficiency combatting of MDR bacteria is in urgent demand. Hydrogen (H(2)) is a small gas with a high reducing ability, and plenty of recent studies have demonstrated its therapeutic effect on many diseases. However, the antibacterial effectiveness and mechanism of H(2) against MDR bacteria are still unknown. In the present work, using PdH nanohydride with a temperature responsive H(2)-releasing property as the H(2) source, we demonstrated that H(2) was not only able to inhibit the growth of normal Staphylococcus aureus (S. aureus), but could also effectively eliminate single drug resistant S. aureus (CRSA) and multidrug resistant S. aureus (MRSA), as well as the biofilms formed by those bacteria. Moreover, an in-depth mechanism regarding the anti-antibiotic-resistance activity of H(2) was elucidated by us, in which H(2) exerted its antibacterial effect by firstly causing severe membrane damage, followed by boosting generation of intracellular ROS, which subsequently triggered DNA damage and finally led to bacterial death. The proposed mechanism was further verified by genomic analysis, where a cluster of genes related to bacterial membrane integrity, biofilm formation, metabolism and DNA functions was significantly perturbed by the released H(2). In particular, H(2) boosted intracellular ROS generation by destroying the redox homeostasis of bacterial metabolism. More importantly, we revealed that H(2) was able to alleviate the antibiotic resistance of CRSA and MRSA by significantly down-regulating the expression of many drug-resistant genes, e.g. the norG gene of CRSA, and fmtA, gpsB, sarA and marR genes of MRSA, as well as reducing the minimal inhibitory concentration (MIC) of ciprofloxacin/ampicillin against CRSA/MRSA. The findings in our work suggested that H(2) therapy is a promising tool for combating antibiotic-resistant bacteria.202336655922
898070.9944Omics analyses indicate sdhC/D act as hubs of early response of E. coli to antibiotics. In recent years, the phenomenon of microbial resistance has become increasingly serious. The generation of reactive oxygen species (ROS) during the bactericidal process of antibiotics has attracted great interest, but little research has been done on the generation of ROS in the early stage of antibiotic action. We confirmed the rapid production of ROS by flow cytometry and transmission electron microscopy (TEM). GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analysis indicated that the oxidative phosphorylation pathway is the key pathway of ROS production. Protein-protein interaction (PPI) network results indicate that sdhC/D are key genes in the oxidative phosphorylation pathway. The overexpression of sdhC/D resulted in a lower survival rate than the control strain after antibiotic treatments, which might be due to excess ROS induced by sdhC/D overexpression. The production of superoxide anion in the overexpress strain was significantly higher than that in the control strain, which further verified the importance of sdhC/D in the ROS release of bacteria. Current results showed that bacteria produce large amounts of ROS in the early stage of gentamicin and ampicillin action, and the regulation patterns of genes in the key pathway were consistent. sdhC/D are key genes in the early ROS release process of bacteria. Our study provides a basis for the search of ROS-related enhancers of antimicrobial action.202235933647
897380.9944Enhanced myco-synthesis of selenium and zinc oxide nanoparticles and evaluating their anticancer activities and role against antibiotic resistance genes in certain bacterial strains. BACKGROUND: In an array to check microbial resistance against generally used antibiotics, it is essential to create innovative and efficient antimicrobial agents. Therefore, nanoparticles (NPs) with their antimicrobial activities describe an effective solution. In this study, we synthesized Selenium nanoparticles (Se-NPs) and zinc oxide nanoparticles (ZnO-NPs) using Alternaria alternata fungus, then their characterization were evaluated using several techniques. RESULTS: We explored the potential of antimicrobial impact of Se-NPs and ZnO-NPs against negative and positive grams antibiotic resistance bacterial strains in combination with penicillin, Ceftriaxone and Cefipime. Moreover, antibiotic resistance gene expression was assessed after those treatments. The results demonstrated that Se-NPs and ZnO-NPs displayed antibacterial properties, while the expression of antibiotic resistance genes decreased when exposed to a combination of NPs and antibiotics. This suggests the presence of both synergistic and additive effects in these treatments. Furthermore, the cytotoxic effects of Se-NPs and ZnO-NPs were assessed, revealing their potent anticancer properties against MCF-7, A549, and HepG2 cancer cells and lower cytotoxic values for HFB-4 standard cell line. Ultimately, the production efficiency of both NPs was enhanced through gamma irradiation. CONCLUSIONS: According to the results, it seems that the green synthesis of Se-NPs and ZnO-NPs promotes environmental sustainability and cost-effective approach. This study provides insights into the development of new antibacterial and anticancer agents . The eco-friendly production of nanoparticles suggests also a sustainable approach to combating bacteria resistant to antibiotics.202541046259
818990.9944Engineering nanoparticles to silence bacterial communication. The alarming spread of bacterial resistance to traditional antibiotics has warranted the study of alternative antimicrobial agents. Quorum sensing (QS) is a chemical cell-to-cell communication mechanism utilized by bacteria to coordinate group behaviors and establish infections. QS is integral to bacterial survival, and therefore provides a unique target for antimicrobial therapy. In this study, silicon dioxide nanoparticles (Si-NP) were engineered to target the signaling molecules [i.e., acylhomoserine lactones (HSLs)] used for QS in order to halt bacterial communication. Specifically, when Si-NP were surface functionalized with β-cyclodextrin (β-CD), then added to cultures of bacteria (Vibrio fischeri), whose luminous output depends upon HSL-mediated QS, the cell-to-cell communication was dramatically reduced. Reductions in luminescence were further verified by quantitative polymerase chain reaction (qPCR) analyses of luminescence genes. Binding of HSLs to Si-NPs was examined using nuclear magnetic resonance (NMR) spectroscopy. The results indicated that by delivering high concentrations of engineered NPs with associated quenching compounds, the chemical signals were removed from the immediate bacterial environment. In actively-metabolizing cultures, this treatment blocked the ability of bacteria to communicate and regulate QS, effectively silencing and isolating the cells. Si-NPs provide a scaffold and critical stepping-stone for more pointed developments in antimicrobial therapy, especially with regard to QS-a target that will reduce resistance pressures imposed by traditional antibiotics.201525806030
622100.9943Small-Molecule Antibiotics Inhibiting tRNA-Regulated Gene Expression Is a Viable Strategy for Targeting Gram-Positive Bacteria. Bacterial infections and the rise of antibiotic resistance, especially multidrug resistance, have generated a clear need for discovery of novel therapeutics. We demonstrated that a small-molecule drug, PKZ18, targets the T-box mechanism and inhibits bacterial growth. The T-box is a structurally conserved riboswitch-like gene regulator in the 5' untranslated region (UTR) of numerous essential genes of Gram-positive bacteria. T-boxes are stabilized by cognate, unacylated tRNA ligands, allowing the formation of an antiterminator hairpin in the mRNA that enables transcription of the gene. In the absence of an unacylated cognate tRNA, transcription is halted due to the formation of a thermodynamically more stable terminator hairpin. PKZ18 targets the site of the codon-anticodon interaction of the conserved stem I and reduces T-box-controlled gene expression. Here, we show that novel analogs of PKZ18 have improved MICs, bactericidal effects against methicillin-resistant Staphylococcus aureus (MRSA), and increased efficacy in nutrient-limiting conditions. The analogs have reduced cytotoxicity against eukaryotic cells compared to PKZ18. The PKZ18 analogs acted synergistically with aminoglycosides to significantly enhance the efficacy of the analogs and aminoglycosides, further increasing their therapeutic windows. RNA sequencing showed that the analog PKZ18-22 affects expression of 8 of 12 T-box controlled genes in a statistically significant manner, but not other 5'-UTR regulated genes in MRSA. Very low levels of resistance further support the existence of multiple T-box targets for PKZ18 analogs in the cell. Together, the multiple targets, low resistance, and synergy make PKZ18 analogs promising drugs for development and future clinical applications.202033077662
8909110.9943Nanoalumina triggers the antibiotic persistence of Escherichia coli through quorum sensing regulators lrsF and qseB. Nanomaterials with bactericidal effects might provide novel strategies against bacteria. However, some bacteria can survive despite the exposure to nanomaterials, which challenges the safety of antibacterial nanomaterials. Here, we used a high dose of antibiotics to kill the E. coli. that survived under different concentrations of nanoalumina treatment to screen persisters, and found that nanoalumina could significantly trigger persisters formation. Treatment with 50 mg/L nanoalumina for 4 h resulted in the formation of (0.084 ± 0.005) % persisters. Both reactive oxygen species (ROS) and toxin-antitoxin (TA) system were involved in persisters formation. Interestingly, RT-PCR analysis and knockout of the five genes related to ROS and TA confirmed that only hipB was associated with the formation of persisters, suggesting the involvement of other mechanisms. We further identified 73 differentially expressed genes by transcriptome sequencing and analyzed them with bioinformatics tools. We selected six candidate genes and verified that five of them closely related to quorum sensing (QS) that were involved in persisters formation, and further validated that the coexpression of QS factors lrsF and qseB was a novel pathway for persisters. Our findings provided a better understanding on the emergence of bacterial persistence and the microbial behavior under nanomaterials exposure.202235739728
8769120.9943Transgenic soybean of GsMYB10 shapes rhizosphere microbes to promote resistance to aluminum (Al) toxicity. Plant resistance genes could affect rhizosphere microbiota, which in turn enhanced plant resistance to stresses. Our previous study found that overexpression of the GsMYB10 gene led to enhanced tolerance of soybean plants to aluminum (Al) toxicity. However, whether GsMYB10 gene could regulate rhizosphere microbiota to mitigate Al toxicity remains unclear. Here, we analyzed the rhizosphere microbiomes of HC6 soybean (WT) and transgenic soybean (trans-GsMYB10) at three Al concentrations, and constructed three different synthetic microbial communities (SynComs), including bacterial, fungal and cross-kingdom (bacteria and fungi) SynComs to verify their role in improving Al tolerance of soybean. Trans-GsMYB10 shaped the rhizosphere microbial communities and harbored some beneficial microbes, such as Bacillus, Aspergillus and Talaromyces under Al toxicity. Fungal and cross-kingdom SynComs showed a more effective role than the bacterial one in resistance to Al stress, and these SynComs helped soybean resist Al toxicity via affecting some functional genes that involved cell wall biosynthesis and organic acid transport etc. Overall, this study reveals the mechanism of soybean functional genes regulating the synergistic resistance of rhizosphere microbiota and plants to Al toxicity, and also highlights the possibility of focusing on the rhizobial microbial community as a potential molecular breeding target to produce crops.202337187122
8490130.9943Unveiling the kinetics and mechanism of carbonate radicals in antibiotic resistance dissemination. The escalating contamination of antibiotic resistant bacteria (ARB) and antibiotic resistance genes (ARGs) in aquatic systems has driven extensive investigations into their interactions with reactive intermediates. However, the reaction kinetics and mechanisms underlying the degradation of ARB and ARGs by CO(3)(•-) remain unelucidated. This study quantifies the reaction rate constants between CO(3)(•-) and ARB, ARGs, and critical biomolecules including extracellular polymeric substances, phospholipids, amino acids, and deoxynucleotides. Results demonstrate negligible CO(3)(•-) reactivity with phospholipids and amino acids (< 10(5) M(-1)·s(-1)), yet remarkably high reaction rates (∼10(7) M(-1)·s(-1)) with ARB, ARGs and deoxynucleotides. Mechanistic studies demonstrate that CO(3)(•-) enhances membrane fluidity by attenuating inter-lipid interactions and reducing lipid ordering (Δη = -60.44 %), thereby driving transmembrane co-transport with HCO(3)⁻. Notably, CO(3)(•-) exhibits an extended reaction radius (1.30-2.31 μm, far exceeding typical membrane-targeting radicals) and exploits its low membrane affinity to achieve deep cellular penetration. Within cells, it selectively oxidizes biomolecules, primarily via deoxyguanosine modification, inducing ARGs damage and systemic biomolecular dysregulation. Integrated transcriptomic and metabolomic analyses confirm these genotoxic impacts, revealing perturbations at transcriptional regulation and metabolic pathway levels. These results establish CO(3)(•-) as a potential key agent in suppressing antibiotic resistance dissemination, resolving a critical knowledge gap in environmental radical-ARB/ARGs interactions.202541101271
715140.9943Transcription tuned by S-nitrosylation underlies a mechanism for Staphylococcus aureus to circumvent vancomycin killing. Treatment of Staphylococcus aureus infections is a constant challenge due to emerging resistance to vancomycin, a last-resort drug. S-nitrosylation, the covalent attachment of a nitric oxide (NO) group to a cysteine thiol, mediates redox-based signaling for eukaryotic cellular functions. However, its role in bacteria is largely unknown. Here, proteomic analysis revealed that S-nitrosylation is a prominent growth feature of vancomycin-intermediate S. aureus. Deletion of NO synthase (NOS) or removal of S-nitrosylation from the redox-sensitive regulator MgrA or WalR resulted in thinner cell walls and increased vancomycin susceptibility, which was due to attenuated promoter binding and released repression of genes involved in cell wall metabolism. These genes failed to respond to H(2)O(2)-induced oxidation, suggesting distinct transcriptional responses to alternative modifications of the cysteine residue. Furthermore, treatment with a NOS inhibitor significantly decreased vancomycin resistance in S. aureus. This study reveals that transcriptional regulation via S-nitrosylation underlies a mechanism for NO-mediated bacterial antibiotic resistance.202337085493
8491150.9943Hormesis-like effects of black phosphorus nanosheets on the spread of multiple antibiotic resistance genes. The production scalability and increasing demand for black phosphorus nanosheets (BPNSs) inevitably lead to environmental leakage. Although BPNSs' ecotoxicological effects have been demonstrated, their indirect health risks, such as inducing increased resistance in pathogenic bacteria, are often overlooked. This study explores the influence of BPNSs on the horizontal gene transfer of antibiotic resistance genes (ARGs) facilitated by the RP4 plasmid, which carries multiple resistance genes. The results indicated that BPNSs exhibited concentration-dependent hormesis-like effects on bacterial conjugation gene transfer. Specifically, at sub-inhibitory concentrations (0.0001-1 mg/L), BPNSs promoted both intra- and intergeneric conjugative transfer, demonstrating an initial increase followed by a decline, with transfer rates rising by 1.5-3.1-fold and 1.5-3.3-fold, respectively. BPNSs were found to induce reactive oxygen species (ROS) production, increase malondialdehyde levels, and trigger the SOS response, enhancing plasmid uptake. Additionally, BPNSs increased membrane permeability by forming pores and upregulating outer membrane porins (OMPs) genes. At higher BPNSs concentrations (0.1-1 mg/L), conjugative frequency was inhibited due to the disruption of the cellular antioxidant system and changes in the adsorption process. These findings underscore the influence of BPNSs on the conjugative transfer of ARGs, complementing current knowledge of the biotoxicity and potential ecological risks associated with BPNSs.202539827804
8540160.9943Metagenomic insights into the mechanism for the rapid enrichment and high stability of Candidatus Brocadia facilitated by Fe(Ⅲ). The rapid enrichment of anammox bacteria and its fragile resistance to adverse environment are the critical problems facing of anammox processes. As an abundant component in anammox bacteria, iron has been proved to promote the activity and growth of anammox bacteria in the mature anammox systems, but the functional and metabolic profiles in Fe(III) enhanced emerging anammox systems have not been evaluated. Results indicated that the relative abundance of functional genes involved in oxidative phosphorylation, nitrogen metabolism, cofactors synthesis, and extracellular polymers synthesis pathways was significantly promoted in the system added with 5 mg/L Fe(III) (R5). These enhanced pathways were crucial to energy generation, nitrogen removal, cell activity and proliferation, and microbial self-defense, thereby accelerating the enrichment of anammox bacteria Ca. Brocadia and facilitating their resistance to adverse environments. Microbial community analysis showed that the proportion of Ca. Brocadia in R5 also increased to 64.42 %. Hence, R5 could adapt rapidly to the increased nitrogen loading rate and increase the nitrogen removal rate by 108 % compared to the system without Fe(III) addition. However, the addition of 10 and 20 mg/L Fe(III) showed inhibitory effects on the growth and activity of anammox bacteria, which exhibited the lower relative abundance of Ca. Brocadia and unstable or even collapsed nitrogen removal performance. This study not only clarified the concentration range of Fe(III) that promoted and inhibited the enrichment of anammox bacteria, but also deepened our understanding of the functional and metabolic mechanisms underlying enhanced enrichment of anammox bacteria by Fe(III), providing a potential strategy to hasten the start-up of anammox from conventional activated sludge.202438309072
8976170.9942Biosynthesis of H(2)S and Siderophores Targeting Gram-Negative Bacterial Resistance to Reactive Oxygen Species. Reactive oxygen species (ROS) are a promising alternative bactericide. However, it is questioned that bacteria can potentially develop resistance to ROS, similar to their resistance against antibiotics and silver. Herein, it is reported that Gram-negative bacteria, including Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae, develop resistance to ROS after six repeated exposures. Notably, ROS minimum inhibitory concentration of Pseudomonas aeruginosa significantly increases to 256-fold after ten passages. The resistance mechanism predominantly originates from the intensified biosynthesis of the highly reductive hydrogen sulfide (H(2)S) and pyoverdine (PVD) siderophores, effectively neutralizing ROS. Simultaneously, PVD transports Fe(3+) from the extracellular space into the bacteria, releasing H(2)S bound to Fe(3+) and enhancing ROS scavenging. Additionally, the enhanced outer membrane (OM) biogenesis establishes a robust OM barrier, impeding ROS penetration. The acquired resistance to ROS can be significantly reduced by incorporating additional Fe(3+) into the culture medium or disrupting the H(2)S biosynthetic gene. These observations suggest that careful consideration is required when utilizing ROS against Gram-negative bacteria. It is anticipated that understanding this resistance mechanism can inform the development of future antimicrobial agents, particularly for Gram-negative bacteria.202540948366
8767180.9942Poly-γ-glutamic acid enhanced the drought resistance of maize by improving photosynthesis and affecting the rhizosphere microbial community. BACKGROUND: Compared with other abiotic stresses, drought stress causes serious crop yield reductions. Poly-γ-glutamic acid (γ-PGA), as an environmentally friendly biomacromolecule, plays an important role in plant growth and regulation. RESULTS: In this project, the effect of exogenous application of γ-PGA on drought tolerance of maize (Zea mays. L) and its mechanism were studied. Drought dramatically inhibited the growth and development of maize, but the exogenous application of γ-PGA significantly increased the dry weight of maize, the contents of ABA, soluble sugar, proline, and chlorophyll, and the photosynthetic rate under severe drought stress. RNA-seq data showed that γ-PGA may enhance drought resistance in maize by affecting the expression of ABA biosynthesis, signal transduction, and photosynthesis-related genes and other stress-responsive genes, which was also confirmed by RT-PCR and promoter motif analysis. In addition, diversity and structure analysis of the rhizosphere soil bacterial community demonstrated that γ-PGA enriched plant growth promoting bacteria such as Actinobacteria, Chloroflexi, Firmicutes, Alphaproteobacteria and Deltaproteobacteria. Moreover, γ-PGA significantly improved root development, urease activity and the ABA contents of maize rhizospheric soil under drought stress. This study emphasized the possibility of using γ-PGA to improve crop drought resistance and the soil environment under drought conditions and revealed its preliminary mechanism. CONCLUSIONS: Exogenous application of poly-γ-glutamic acid could significantly enhance the drought resistance of maize by improving photosynthesis, and root development and affecting the rhizosphere microbial community.202234979944
8341190.9942Mutagenesis and Resistance Development of Bacteria Challenged by Silver Nanoparticles. Because of their extremely broad spectrum and strong biocidal power, nanoparticles of metals, especially silver (AgNPs), have been widely applied as effective antimicrobial agents against bacteria, fungi, and so on. However, the mutagenic effects of AgNPs and resistance mechanisms of target cells remain controversial. In this study, we discover that AgNPs do not speed up resistance mutation generation by accelerating genome-wide mutation rate of the target bacterium Escherichia coli. AgNPs-treated bacteria also show decreased expression in quorum sensing (QS), one of the major mechanisms leading to population-level drug resistance in microbes. Nonetheless, these nanomaterials are not immune to resistance development by bacteria. Gene expression analysis, experimental evolution in response to sublethal or bactericidal AgNPs treatments, and gene editing reveal that bacteria acquire resistance mainly through two-component regulatory systems, especially those involved in metal detoxification, osmoregulation, and energy metabolism. Although these findings imply low mutagenic risks of nanomaterial-based antimicrobial agents, they also highlight the capacity for bacteria to evolve resistance.202236094196