# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 4 | 0 | 0.9528 | Bacteria deplete deoxynucleotides to defend against bacteriophage infection. DNA viruses and retroviruses consume large quantities of deoxynucleotides (dNTPs) when replicating. The human antiviral factor SAMHD1 takes advantage of this vulnerability in the viral lifecycle, and inhibits viral replication by degrading dNTPs into their constituent deoxynucleosides and inorganic phosphate. Here, we report that bacteria use a similar strategy to defend against bacteriophage infection. We identify a family of defensive bacterial deoxycytidine triphosphate (dCTP) deaminase proteins that convert dCTP into deoxyuracil nucleotides in response to phage infection. We also identify a family of phage resistance genes that encode deoxyguanosine triphosphatase (dGTPase) enzymes, which degrade dGTP into phosphate-free deoxyguanosine and are distant homologues of human SAMHD1. Our results suggest that bacterial defensive proteins deplete specific deoxynucleotides (either dCTP or dGTP) from the nucleotide pool during phage infection, thus starving the phage of an essential DNA building block and halting its replication. Our study shows that manipulation of the dNTP pool is a potent antiviral strategy shared by both prokaryotes and eukaryotes. | 2022 | 35817891 |
| 103 | 1 | 0.9378 | IL-1 receptor regulates S100A8/A9-dependent keratinocyte resistance to bacterial invasion. Previously, we reported that epithelial cells respond to exogenous interleukin (IL)-1α by increasing expression of several genes involved in the host response to microbes, including the antimicrobial protein complex calprotectin (S100A8/A9). Given that S100A8/A9 protects epithelial cells against invading bacteria, we studied whether IL-1α augments S100A8/A9-dependent resistance to bacterial invasion of oral keratinocytes. When inoculated with Listeria monocytogenes, human buccal epithelial (TR146) cells expressed and released IL-1α. Subsequently, IL-1α-containing media from Listeria-infected cells increased S100A8/A9 gene expression in naïve TR146 cells an IL-1 receptor (IL-1R)-dependent manner. Incubation with exogenous IL-1α decreased Listeria invasion into TR146 cells, whereas invasion increased with IL-1R antagonist. Conversely, when S100A8/A9 genes were knocked down using short hairpin RNA (shRNA), TR146 cells responded to exogenous IL-1α with increased intracellular bacteria. These data strongly suggest that infected epithelial cells release IL-1α to signal neighboring keratinocytes in a paracrine manner, promoting S100A8/A9-dependent resistance to invasive L. monocytogenes. | 2012 | 22031183 |
| 7871 | 2 | 0.9368 | Effects of different quaternary ammonium compounds on intracellular and extracellular resistance genes in nitrification systems under the pre-contamination of benzalkyl dimethylammonium compounds. As the harm of benzalkyl dimethylammonium compounds (BACs) on human health and environment was discovered, alkyltrimethyl ammonium compound (ATMAC) and dialkyldimethyl ammonium compound (DADMAC), which belong to quaternary ammonium compounds (QACs), were likely to replace BACs as the main disinfectants. This study simulated the iterative use of QACs to explore their impact on resistance genes (RGs) in nitrification systems pre-contaminated by BACs. ATMAC could initiate and maintain partial nitrification. DADMAC generated higher levels of reactive oxygen species and lactate dehydrogenase, leading to increased biological toxicity in bacteria. The abundance of intracellular RGs of sludge was higher with the stress of QACs. DADMAC also induced higher extracellular polymeric substance secretion. Moreover, it facilitated the transfer of RGs from sludge to water, with ATMAC disseminating RGs through si-tnpA-04 and DADMAC through si-intI1. Sediminibacterium might be potential hosts for RGs. This study offered insights into disinfectant usage in the post-COVID-19 era. | 2025 | 39612960 |
| 41 | 3 | 0.9363 | Rice WRKY13 regulates cross talk between abiotic and biotic stress signaling pathways by selective binding to different cis-elements. Plants use a complex signal transduction network to regulate their adaptation to the ever-changing environment. Rice (Oryza sativa) WRKY13 plays a vital role in the cross talk between abiotic and biotic stress signaling pathways by suppressing abiotic stress resistance and activating disease resistance. However, it is not clear how WRKY13 directly regulates this cross talk. Here, we show that WRKY13 is a transcriptional repressor. During the rice responses to drought stress and bacterial infection, WRKY13 selectively bound to certain site- and sequence-specific cis-elements on the promoters of SNAC1 (for STRESS RESPONSIVE NO APICAL MERISTEM, ARABIDOPSIS TRANSCRIPTION ACTIVATION FACTOR1/2, CUP-SHAPED COTYLEDON), the overexpression of which increases drought resistance, and WRKY45-1, the knockout of which increases both bacterial disease and drought resistance. WRKY13 also bound to two cis-elements of its native promoter to autoregulate the balance of its gene expression in different physiological activities. WRKY13 was induced in leaf vascular tissue, where bacteria proliferate, during infection, and in guard cells, where the transcriptional factor SNAC1 enhances drought resistance, during both bacterial infection and drought stress. These results suggest that WRKY13 regulates the antagonistic cross talk between drought and disease resistance pathways by directly suppressing SNAC1 and WRKY45-1 and autoregulating its own expression via site- and sequence-specific cis-elements on the promoters of these genes in vascular tissue where bacteria proliferate and guard cells where the transcriptional factor SNAC1 mediates drought resistance by promoting stomatal closure. | 2013 | 24130197 |
| 8490 | 4 | 0.9361 | Unveiling 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. | 2025 | 41101271 |
| 608 | 5 | 0.9356 | Entamoeba histolytica Adaption to Auranofin: A Phenotypic and Multi-Omics Characterization. Auranofin (AF), an antirheumatic agent, targets mammalian thioredoxin reductase (TrxR), an important enzyme controlling redox homeostasis. AF is also highly effective against a diversity of pathogenic bacteria and protozoan parasites. Here, we report on the resistance of the parasite Entamoeba histolytica to 2 µM of AF that was acquired by gradual exposure of the parasite to an increasing amount of the drug. AF-adapted E. histolytica trophozoites (AFAT) have impaired growth and cytopathic activity, and are more sensitive to oxidative stress (OS), nitrosative stress (NS), and metronidazole (MNZ) than wild type (WT) trophozoites. Integrated transcriptomics and redoxomics analyses showed that many upregulated genes in AFAT, including genes encoding for dehydrogenase and cytoskeletal proteins, have their product oxidized in wild type trophozoites exposed to AF (acute AF trophozoites) but not in AFAT. We also showed that the level of reactive oxygen species (ROS) and oxidized proteins (OXs) in AFAT is lower than that in acute AF trophozoites. Overexpression of E. histolytica TrxR (EhTrxR) did not protect the parasite against AF, which suggests that EhTrxR is not central to the mechanism of adaptation to AF. | 2021 | 34439488 |
| 7872 | 6 | 0.9354 | Quaternary ammonium compounds promoted anoxic sludge granulation and altered propagation risk of intracellular and extracellular antibiotic resistance genes. Surfactants could influence sludge morphology and disinfectants were linked to antibiotic resistance genes (ARGs). Thus, the response of activated sludge and ARGs to long-term quaternary ammonium compounds (QACs) exposure required further investigation, which is a popular surfactant and disinfectant. Here, three sequencing batch reactors were fed with 5 mg/L most frequently detected QACs (dodecyl trimethyl ammonium chloride (ATMAC C12), dodecyl benzyl dimethyl ammonium chloride (BAC C12) and didodecyl dimethyl ammonium chloride (DADMAC C12)) for 180 d. The long-term inhibitory effect on denitrification ranked: DADMAC C12 > BAC C12 > ATMAC C12. Besides, obvious granular sludge promoted by the increase of α-Helix/(β-Sheet + Random coil) appeared in DADMAC C12 system. Moreover, intracellular ARGs increased when denitrification systems encountered QACs acutely but decreased in systems chronically exposed to QACs. Although replication and repair metabolism in ATMAC C12 system was higher, ATMAC C12 significantly promoted proliferation of extracellular ARGs. It was noteworthy that the propagation risk of extracellular ARGs in sludge increased significantly during sludge granulation process, and intracellular sul2 genes in sludge and water both increased with the granular diameter in DADMAC C12 system. The universal utilization of QACs may enhance antibiotic resistance of bacteria in wastewater treatment plants, deserving more attention. | 2023 | 36444811 |
| 7877 | 7 | 0.9351 | External circuit loading mode regulates anode biofilm electrochemistry and pollutants removal in microbial fuel cells. This study investigated the effects of different external circuit loading mode on pollutants removal and power generation in microbial fuel cells (MFC). The results indicated that MFC exhibited distinct characteristics of higher maximum power density (P(max)) (named MFC-HP) and lower P(max) (named MFC-LP). And the capacitive properties of bioanodes may affect anodic electrochemistry. Reducing external load to align with the internal resistance increased P(max) of MFC-LP by 54.47 %, without no obvious effect on MFC-HP. However, intermittent external resistance loading (IER) mitigated the biotoxic effects of sulfamethoxazole (SMX) (a persistent organic pollutant) on chemical oxygen demand (COD) and NH(4)(+)-N removal and maintained high P(max) (424.33 mW/m(2)) in MFC-HP. Meanwhile, IER mode enriched electrochemically active bacteria (EAB) and environmental adaptive bacteria Advenella, which may reduce antibiotic resistance genes (ARGs) accumulation. This study suggested that the external circuit control can be effective means to regulate electrochemical characteristics and pollutants removal performance of MFC. | 2024 | 39153696 |
| 8487 | 8 | 0.9351 | 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 |
| 607 | 9 | 0.9349 | A novel copper-sensing two-component system for inducing Dsb gene expression in bacteria. In nature, bacteria must sense copper and tightly regulate gene expression to evade copper toxicity. Here, we identify a new copper-responsive two-component system named DsbRS in the important human pathogen Pseudomonas aeruginosa; in this system, DsbS is a sensor histidine kinase, and DsbR, its cognate response regulator, directly induces the transcription of genes involved in protein disulfide bond formation (Dsb) (i.e., the dsbDEG operon and dsbB). In the absence of copper, DsbS acts as a phosphatase toward DsbR, thus blocking the transcription of Dsb genes. In the presence of copper, the metal ion directly binds to the sensor domain of DsbS, and the Cys82 residue plays a critical role in this process. The copper-binding behavior appears to inhibit the phosphatase activity of DsbS, leading to the activation of DsbR. The copper resistance of the dsbRS knock-out mutant is restored by the ectopic expression of the dsbDEG operon, which is a DsbRS major target. Strikingly, cognates of the dsbRS-dsbDEG pair are widely distributed across eubacteria. In addition, a DsbR-binding site, which contains the consensus sequence 5'-TTA-N(8)-TTAA-3', is detected in the promoter region of dsbDEG homologs in these species. These findings suggest that the regulation of Dsb genes by DsbRS represents a novel mechanism by which bacterial cells cope with copper stress. | 2022 | 36546013 |
| 7887 | 10 | 0.9347 | 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 |
| 36 | 11 | 0.9341 | Bacillus amyloliquefaciens SN16-1-Induced Resistance System of the Tomato against Rhizoctonia solani. Tomato (Solanum lycopersicum), as an important economical vegetable, is often infected with Rhizoctonia solani, which results in a substantial reduction in production. Therefore, the molecular mechanism of biocontrol microorganisms assisting tomato to resist pathogens is worth exploring. Here, we use Bacillus amyloliquefaciens SN16-1 as biocontrol bacteria, and employed RNA-Seq technology to study tomato gene and defense-signaling pathways expression. Gene Ontology (GO) analyses showed that an oxidation-reduction process, peptidase regulator activity, and oxidoreductase activity were predominant. Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses showed that phenylpropanoid biosynthesis, biosynthesis of unsaturated fatty acids, aldosterone synthesis and secretion, and phototransduction were significantly enriched. SN16-1 activated defenses in the tomato via systemic-acquired resistance (which depends on the salicylic acid signaling pathway), rather than classic induction of systemic resistance. The genes induced by SN16-1 included transcription factors, plant hormones (ethylene, auxin, abscisic acid, and gibberellin), receptor-like kinases, heat shock proteins, and defense proteins. SN16-1 rarely activated pathogenesis-related proteins, but most pathogenesis-related proteins were induced in the presence of the pathogens. In addition, the molecular mechanisms of the response of tomatoes to SN16-1 and R. solani RS520 were significantly different. | 2021 | 35055983 |
| 7882 | 12 | 0.9341 | Insights into antibiotic resistance gene abundances and regulatory mechanisms induced by ionic liquids during composting. This study investigated the regulatory mechanism of the evolution of antibiotic resistance genes (ARGs) during the composting process with sawdust and cow manure as raw materials using ionic liquids (ILs) pretreatment. The results showed that genes of MLS, chloramphenicol, tetracycline, beta - lactam as composting gradually decreased. From day0 to day3, MLS in control group (CK) and experimental group (T) decreased by 25.62% and 26.66%, respectively. Tetracycline decreased by 7.21% in CK and by 7.86% in T. Chloramphenicol decreased by 2.85% in CK and 3.34% in T. Beta-lactam decreased by 1.95% in Ck and by 3.69% in T. Mechanism studies have shown that ILs can effectively decompose extracellular polymeric substances (EPS) and enhance lactose dehydrogenase (LDH) release, resulting in ARGs release and elimination. Meanwhile, ILs pretreatment can inhibit growth of some ARGs hosts, especially Firmicutes, resulting in decreased ARGs. Moreover, metabolic pathways and related genes take part in ARGs transmission were down regulated, leading to decreased ARGs. | 2023 | 37481880 |
| 594 | 13 | 0.9338 | Challenging Xanthomonas campestris with low levels of arsenic mediates cross-protection against oxidant killing. Xanthomonas encounters highly toxic reactive oxygen species (ROS) from many sources, such as those generated by plants against invading bacteria, other soil bacteria and from aerobic respiration. Thus, conditions that alter intracellular ROS levels such as exposure to toxic metalloids would have profound effects on bacterial physiology. Here, we report that exposure of Xanthomonas campestris pv. phaseoli (Xp) to low levels of arsenic induces physiological cross-protection against killing by H(2)O(2) and organic hydroperoxide but not a superoxide generator. Cross-protection against H(2)O(2) and organic hydroperoxide toxicity was due to increased expression of genes encoding major peroxide-metabolizing enzymes such as alkyl hydroperoxide reductase (AhpC), catalase (KatA) and organic hydroperoxide resistance protein (Ohr). Arsenic-induced protection against H(2)O(2) and organic hydroperoxide requires the peroxide stress response regulators, OxyR and OhrR, respectively. Moreover, analyses of double mutants of the major H(2)O(2) and organic hyproperoxide-scavenging enzymes, Xp ahpC katA and Xp ahpC ohr, respectively, suggested the existence of unidentified OxyR- and OhrR-regulated genes that are involved in arsenic-induced resistance to H(2)O(2) and organic hyproperoxide killing in Xp. These arsenic-induced physiological alterations could play an important role in bacterial survival both in the soil environment and during plant-pathogen interactions. | 2006 | 16907748 |
| 801 | 14 | 0.9338 | Redox-sensitive transcriptional regulator SoxR directly controls antibiotic production, development and thiol-oxidative stress response in Streptomyces avermitilis. The redox-sensitive transcriptional regulator SoxR is conserved in bacteria. Its role in mediating protective response to various oxidative stresses in Escherichia coli and related enteric bacteria has been well established. However, functions and regulatory mechanisms of SoxR in filamentous Streptomyces, which produce half of known antibiotics, are unclear. We report here that SoxR pleiotropically regulates antibiotic production, morphological development, primary metabolism and thiol-oxidative stress response in industrially important species Streptomyces avermitilis. SoxR stimulated avermectin production by directly activating ave structural genes. Four genes (sav_3956, sav_4018, sav_5665 and sav_7218) that are homologous to targets of S. coelicolor SoxR are targeted by S. avermitilis SoxR. A consensus 18-nt SoxR-binding site, 5'-VSYCNVVMHNKVKDGMGB-3', was identified in promoter regions of sav_3956, sav_4018, sav_5665, sav_7218 and target ave genes, leading to prediction of the SoxR regulon and confirmation of 11 new targets involved in development (ftsH), oligomycin A biosynthesis (olmRI), primary metabolism (metB, sav_1623, plcA, nirB, thiG, ndh2), transport (smoE) and regulatory function (sig57, sav_7278). SoxR also directly activated three key developmental genes (amfC, whiB and ftsZ) and promoted resistance of S. avermitilis to thiol-oxidative stress through activation of target trx and msh genes. Overexpression of soxR notably enhanced antibiotic production in S. avermitilis and S. coelicolor. Our findings expand our limited knowledge of SoxR and will facilitate improvement of methods for antibiotic overproduction in Streptomyces species. | 2022 | 33951287 |
| 546 | 15 | 0.9338 | Resistance to organic hydroperoxides requires ohr and ohrR genes in Sinorhizobium meliloti. BACKGROUND: Sinorhizobium meliloti is a symbiotic nitrogen-fixing bacterium that elicits nodules on roots of host plants Medicago sativa. During nodule formation bacteria have to withstand oxygen radicals produced by the plant. Resistance to H2O2 and superoxides has been extensively studied in S. meliloti. In contrast resistance to organic peroxides has not been investigated while S. meliloti genome encodes putative organic peroxidases. Organic peroxides are produced by plants and are highly toxic. The resistance to these oxygen radicals has been studied in various bacteria but never in plant nodulating bacteria. RESULTS: In this study we report the characterisation of organic hydroperoxide resistance gene ohr and its regulator ohrR in S. meliloti. The inactivation of ohr affects resistance to cumene and ter-butyl hydroperoxides but not to hydrogen peroxide or menadione in vitro. The expression of ohr and ohrR genes is specifically induced by organic peroxides. OhrR binds to the intergenic region between the divergent genes ohr and ohrR. Two binding sites were characterised. Binding to the operator is prevented by OhrR oxidation that promotes OhrR dimerisation. The inactivation of ohr did not affect symbiosis and nitrogen fixation, suggesting that redundant enzymatic activity exists in this strain. Both ohr and ohrR are expressed in nodules suggesting that they play a role during nitrogen fixation. CONCLUSIONS: This report demonstrates the significant role Ohr and OhrR proteins play in bacterial stress resistance against organic peroxides in S. meliloti. The ohr and ohrR genes are expressed in nodule-inhabiting bacteroids suggesting a role during nodulation. | 2011 | 21569462 |
| 8530 | 16 | 0.9337 | Intrinsic chlorine resistance of bacteria modulated by glutaminyl-tRNA biosynthesis in drinking water supply systems. The existence of chlorine-resistant bacteria (CRB) in drinking water supply systems (DWSSs) results in significant challenges to the biological security of drinking water. However, little is known about the intrinsic chlorine-resistant molecular metabolic mechanism of bacteria in DWSSs. This research explored the microbial interactions and the key metabolic pathways that modulate the chlorine resistance of bacteria in full-scale chloraminated DWSSs. The dominant CRB, including Bdellovibrio, Bradyrhizobium, Peredibacter, Sphingomonas, and Hydrogenophaga, strongly interacted with each other to maintain basic metabolism. A total of 4.21% of the bacterial metabolic pathways were key and specific to chlorine-resistant bacteria. Glutaminyl-tRNA biosynthesis was the dominant metabolic pathway of CRB in the target DWSSs. After chloramine disinfection, the relative abundance of glutamate-tRNA ligase (GlnRS) and the related orthologous genes increased by 10.11% and 14.58%, respectively. The inactivation rate of the GlnRS overexpression strain (81.40%) was lower than that of the wild-type strain (90.11%) after exposure to chloramine. Meanwhile, the growth rate of the GlnRS overexpression strain was higher than that of the wild-type strain. Glutaminyl-tRNA biosynthesis can enhance chlorine resistance in DWSSs. | 2022 | 36084827 |
| 56 | 17 | 0.9337 | 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 |
| 7888 | 18 | 0.9336 | Microecology of aerobic denitrification system construction driven by cyclic stress of sulfamethoxazole. The construction of aerobic denitrification (AD) systems in an antibiotic-stressed environment is a serious challenge. This study investigated strategy of cyclic stress with concentration gradient (5-30 mg/L) of sulfamethoxazole (SMX) in a sequencing batch reactor (SBR), to achieve operation of AD. Total nitrogen removal efficiency of system increased from about 10 % to 95 %. Original response of abundant-rare genera to antibiotics was changed by SMX stress, particularly conditionally rare or abundant taxa (CRAT). AD process depends on synergistic effect of heterotrophic nitrifying aerobic denitrification bacteria (Paracoccus, Thauera, Hypomicrobium, etc). AmoABC, napA, and nirK were functionally co-expressed with multiple antibiotic resistance genes (ARGs) (acrR, ereAB, and mdtO), facilitating AD process. ARGs and TCA cycling synergistically enhance the antioxidant and electron transport capacities of AD process. Antibiotic efflux pump mechanism played an important role in operation of AD. The study provides strong support for regulating activated sludge to achieve in situ AD function. | 2024 | 38710419 |
| 559 | 19 | 0.9336 | Coordinated regulation of chemotaxis and resistance to copper by CsoR in Pseudomonas putida. Copper is an essential enzyme cofactor in bacteria, but excess copper is highly toxic. Bacteria can cope with copper stress by increasing copper resistance and initiating chemorepellent response. However, it remains unclear how bacteria coordinate chemotaxis and resistance to copper. By screening proteins that interacted with the chemotaxis kinase CheA, we identified a copper-binding repressor CsoR that interacted with CheA in Pseudomonas putida. CsoR interacted with the HPT (P1), Dimer (P3), and HATPase_c (P4) domains of CheA and inhibited CheA autophosphorylation, resulting in decreased chemotaxis. The copper-binding of CsoR weakened its interaction with CheA, which relieved the inhibition of chemotaxis by CsoR. In addition, CsoR bound to the promoter of copper-resistance genes to inhibit gene expression, and copper-binding released CsoR from the promoter, leading to increased gene expression and copper resistance. P. putida cells exhibited a chemorepellent response to copper in a CheA-dependent manner, and CsoR inhibited the chemorepellent response to copper. Besides, the CheA-CsoR interaction also existed in proteins from several other bacterial species. Our results revealed a mechanism by which bacteria coordinately regulated chemotaxis and resistance to copper by CsoR. | 2025 | 40197389 |