# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 3739 | 0 | 0.9746 | Survey of drug resistance associated gene mutations in Mycobacterium tuberculosis, ESKAPE and other bacterial species. Tuberculosis treatment includes broad-spectrum antibiotics such as rifampicin, streptomycin and fluoroquinolones, which are also used against other pathogenic bacteria. We developed Drug Resistance Associated Genes database (DRAGdb), a manually curated repository of mutational data of drug resistance associated genes (DRAGs) across ESKAPE (i.e. Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter spp.) pathogens, and other bacteria with a special focus on Mycobacterium tuberculosis (MTB). Analysis of mutations in drug-resistant genes listed in DRAGdb suggested both homoplasy and pleiotropy to be associated with resistance. Homoplasy was observed in six genes namely gidB, gyrA, gyrB, rpoB, rpsL and rrs. For these genes, drug resistance-associated mutations at codon level were conserved in MTB, ESKAPE and many other bacteria. Pleiotropy was exemplified by a single nucleotide mutation that was associated with resistance to amikacin, gentamycin, rifampicin and vancomycin in Staphylococcus aureus. DRAGdb data also revealed that mutations in some genes such as pncA, inhA, katG and embA,B,C were specific to Mycobacterium species. For inhA and pncA, the mutations in the promoter region along with those in coding regions were associated with resistance to isoniazid and pyrazinamide respectively. In summary, the DRAGdb database is a compilation of all the major MTB drug resistance genes across bacterial species, which allows identification of homoplasy and pleiotropy phenomena of DRAGs. | 2020 | 32488120 |
| 347 | 1 | 0.9745 | A novel plasmid gene involved in bacteriophage PRD1 infection and conjugative host-range. PRD1 infects bacteria carrying IncN plasmids by binding to their conjugative pili. Mutations in a plasmid locus kikA close to the pilus region result in PRD1 resistance and reduced conjugation proficiency to Klebsiella but not to Escherichia coli. One of the two genes of kikA is sufficient to restore both normal phenotypes. PRD1 binds to cells carrying the mutant plasmid but fails to inject its genome. | 1996 | 8812786 |
| 337 | 2 | 0.9741 | Effect of nifA product on suppression of Nif- phenotype of gln mutation and constitutive synthesis of nitrogenase in Klebsiella pneumoniae. This paper describes the role of nifA product on the ammonia regulation of nitrogen fixation in K. pneumoniae. A plasmid carrying nifA gene under the promoter of tetracycline resistance gene was constructed. When this nifA carrying plasmid was introduced into a glnAG mutant, the Nif- phenotype of this gln mutant was suppressed. Furthermore, when the plasmid was introduced into the wild type and glnAG mutant, derepression of nitrogenase synthesis in ammonia occurred in both strains and the products of nif genes can be detected by two-dimensional gel electrophoresis in the extracts of these ammonia-grown bacterial cells. The constitutive synthesis of nitrogenase in NH4+ was also demonstrated in free living nitrogen-fixing bacteria, Enterobacter cloacae, when the bacteria received the plasmid carrying nifA gene from K. pneumoniae. | 1983 | 6143398 |
| 9980 | 3 | 0.9740 | A vector for the expression of recombinant monoclonal Fab fragments in bacteria. The availability of genes coding for monoclonal Fab fragments of a desired specificity permits their expression in bacteria and provides a simple method for the generation of good quality reagents. In this paper we describe a new phagemid vector for the production of recombinant Fabs from genes obtained from phage display combinatorial libraries. The phagemid features an antibiotic resistance cassette which, once inserted between the heavy chain fragment and the light chain genes, avoids unwanted recombination and preserves useful restriction sites not affecting the Fab production rate. | 1998 | 9776589 |
| 333 | 4 | 0.9734 | Mutants of Escherichia coli altered in both genes coding for the elongation factor Tu. Genetic analysis of a mutant of Escherichia coli resistant to the antibiotic mocimycin is presented. This resistance is due to alterations in both tuf genes coding for the elongation factor Tu. Mocimycin resistance is recessive. Bacteria carryong only one tuf gene from the resistant mutant are still mocimycin sensitive. If the mutant gene is the tufA gene, the seisitive cells can be made resistant through inactivation of the tufB gene by insertion of the bacteriophage milliunits genome. Conditional mocimycin-resistant mutants ban also be isolated when the tufB gene is altered by an amber or a temperature-sensitive mutation. When only the tufB allele from the original mocimycin-resistant mutant is present, inactivation of the wild-type tufA gene fails to give viable mocimycin-resistant progeny. We conclude that the tufA mutant allele codes for a functional mocimycin-resistant EF-Tu, whereas the mutant tufB gene does not code for a functional product. | 1978 | 360222 |
| 3738 | 5 | 0.9734 | In Silico Prediction of Antibiotic Resistance in Mycobacterium ulcerans Agy99 through Whole Genome Sequence Analysis. Buruli ulcer is an emerging infectious disease caused by Mycobacterium ulcerans that has been reported from 33 countries. Antimicrobial agents either alone or in combination with surgery have been proved to be clinically relevant and therapeutic strategies have been deduced mainly from the empirical experience. The genome sequences of M. ulcerans strain AGY99, M. ulcerans ecovar liflandii, and three Mycobacterium marinum strains were analyzed to predict resistance in these bacteria. Fourteen putative antibiotic resistance genes from different antibiotics classes were predicted in M. ulcerans and mutation in katG (R431G) and pncA (T47A, V125I) genes were detected, that confer resistance to isoniazid and pyrazinamide, respectively. No mutations were detected in rpoB, gyrA, gyrB, rpsL, rrs, emb, ethA, 23S ribosomal RNA genes and promoter region of inhA and ahpC genes associated with resistance. Our results reemphasize the usefulness of in silico analysis for the prediction of antibiotic resistance in fastidious bacteria. | 2017 | 28749770 |
| 528 | 6 | 0.9733 | Effect of dimethyl sulphoxide on the expression of nitrogen fixation in bacteria. Storage in dimethyl sulphoxide (DMSO) of Escherichia coli K12 hybrids carrying nif+ genes from Klebsiella pneumoniae can result in selection of a defective nitrogen-fixing phenotype. Similar results are obtained with E. coli K12 hybrids containing the nitrogen-fixing capacity from Rhizobium trifolii. DMSO appears to affect particular inner membrane proteins associated with energy metabolism in E. coli K12 and four chromosomal regions (chlD, chlG, his and unc) are associated with resistance to DMSO. | 1977 | 332135 |
| 3740 | 7 | 0.9733 | Stp1 Loss of Function Promotes β-Lactam Resistance in Staphylococcus aureus That Is Independent of Classical Genes. β-Lactam resistance in Staphylococcus aureus limits treatment options. Stp1 and Stk1, a serine-threonine phosphatase and kinase, respectively, mediate serine-threonine kinase (STK) signaling. Loss-of-function point mutations in stp1 were detected among laboratory-passaged β-lactam-resistant S. aureus strains lacking mecA and blaZ, the major determinants of β-lactam resistance in the bacteria. Loss of Stp1 function facilitates β-lactam resistance of the bacteria. | 2020 | 32179529 |
| 373 | 8 | 0.9732 | The ybiT gene of Erwinia chrysanthemi codes for a putative ABC transporter and is involved in competitiveness against endophytic bacteria during infection. We investigated the role in bacterial infection of a putative ABC transporter, designated ybiT, of Erwinia chrysanthemi AC4150. The deduced sequence of this gene showed amino acid sequence similarity with other putative ABC transporters of gram-negative bacteria, such as Escherichia coli and Pseudomonas aeruginosa, as well as structural similarity with proteins of Streptomyces spp. involved in resistance to macrolide antibiotics. The gene contiguous to ybiT, designated as pab (putative antibiotic biosynthesis) showed sequence similarity with Pseudomonas and Streptomyces genes involved in the biosynthesis of antibiotics. A ybiT mutant (BT117) was constructed by marker exchange. It retained full virulence in potato tubers and chicory leaves, but it showed reduced ability to compete in planta against the wild-type strain or against selected saprophytic bacteria. These results indicate that the ybiT gene plays a role in the in planta fitness of the bacteria. | 2002 | 11916677 |
| 3744 | 9 | 0.9732 | Vancomycin resistance VanS/VanR two-component systems. Vancomycin is a member of the glycopeptide class of antibiotics. Vancomycin resistance (van) gene clusters are found in human pathogens such as Enterococcus faecalis, Enterococcus faecium and Staphylococcus aureus, glycopeptide-producing actinomycetes such as Amycolotopsis orientalis, Actinoplanes teichomyceticus and Streptomyces toyocaensis and the nonglycopeptide producing actinomycete Streptomyces coelicolor. Expression of the van genes is activated by the VanS/VanR two-component system in response to extracellular glycopeptide antibiotic. Two major types of inducible vancomycin resistance are found in pathogenic bacteria; VanA strains are resistant to vancomycin itself and also to the lipidated glycopeptide teicoplanin, while VanB strains are resistant to vancomycin but sensitive to teicoplanin. Here we discuss the enzymes the van genes encode, the range of different VanS/VanR two-component systems, the biochemistry of VanS/VanR, the nature of the effector ligand(s) recognised by VanS and the evolution of the van cluster. | 2008 | 18792691 |
| 8844 | 10 | 0.9731 | Phage Selective Pressure Reduces Virulence of Hypervirulent Klebsiella pneumoniae Through Mutation of the wzc Gene. Hypervirulent Klebsiella pneumoniae (hvKp), one of the major community-acquired pathogens, can cause invasive infections such as liver abscess. In recent years, bacteriophages have been used in the treatment of K. pneumoniae, but the characteristics of the phage-resistant bacteria produced in the process of phage therapy need to be evaluated. In this study, two Podoviridae phages, hvKpP1 and hvKpP2, were isolated and characterized. In vitro and in vivo experiments demonstrated that the virulence of the resistant bacteria was significantly reduced compared with that of the wild type. Comparative genomic analysis of monoclonal sequencing showed that nucleotide deletion mutations of wzc and wcaJ genes led to phage resistance, and the electron microscopy and mucoviscosity results showed that mutations led to the loss of the capsule. Meanwhile, animal assay indicated that loss of capsule reduced the virulence of hvKp. These findings contribute to a better understanding of bacteriophage therapy, which not only can kill bacteria directly but also can reduce the virulence of bacteria by phage screening. | 2021 | 34690983 |
| 9365 | 11 | 0.9731 | Hypermutability and compensatory adaptation in antibiotic-resistant bacteria. Hypermutable (mutator) bacteria have been associated with the emergence of antibiotic resistance. A simple yet untested prediction is that mutator bacteria are able to compensate more quickly for pleiotropic fitness costs often associated with resistance, resulting in the maintenance of resistance in the absence of antibiotic selection. By using experimental populations of a wild-type and a mutator genotype of the pathogenic bacterium Pseudomonas aeruginosa, we show that mutator bacteria can evolve resistance to antibiotics more rapidly than wild-type bacteria and, crucially, that mutators are better able to compensate for the fitness cost of resistance, to the extent that all costs of resistance were entirely compensated for in mutators. When competed against immigrant antibiotic-susceptible bacteria in the absence of antibiotics, antibiotic resistance remained at a high level in mutator populations but disappeared in wild-type populations. These results suggest that selection for mutations that offset the fitness cost associated with antibiotic resistance may help to explain the high frequency of mutator bacteria and antibiotic resistance observed in chronic infections. | 2010 | 20624092 |
| 3741 | 12 | 0.9729 | The fib locus in Streptococcus pneumoniae is required for peptidoglycan crosslinking and PBP-mediated beta-lactam resistance. Penicillin resistance in pneumococci is mediated by modified penicillin-binding proteins (PBPs) that have decreased affinity to beta-lactams. In high-level penicillin-resistant transformants of the laboratory strain Streptococcus pneumoniae R6 containing various combinations of low-affinity PBPs, disruption of the fib locus results in a collapse of PBP-mediated resistance. In addition, crosslinked muropeptides are highly reduced. The fib operon consists of two genes, fibA and fibB, homologous to Staphylococcus aureus femA/B which are also required for expression of methicillin resistance in this organism. FibA and FibB belong to a family of proteins of Gram-positive bacteria involved in the formation of interpeptide bridges, thus representing interesting new targets for antimicrobial compounds for this group of pathogens. | 2000 | 10867238 |
| 576 | 13 | 0.9729 | Caenorhabditis elegans defective-pharynx and constipated mutants are resistant to Orsay virus infection. C. elegans animals with a compromised pharynx accumulate bacteria in their intestinal lumen and activate a transcriptional response that includes anti-bacterial response genes. In this study, we demonstrate that animals with defective pharynxes are resistant to Orsay virus (OrV) infection. This resistance is observed for animals grown on Escherichia coli OP50 and on Comamonas BIGb0172, a bacterium naturally associated with C. elegans . The viral resistance observed in defective-pharynx mutants does not seem to result from constitutive transcriptional immune responses against viruses. OrV resistance is also observed in mutants with defective defecation, which share with the pharynx-defective perturbations in the regulation of their intestinal contents and altered lipid metabolism. The underlying mechanisms of viral resistance in pharynx- and defecation-defective mutants remain elusive. | 2024 | 38590801 |
| 6222 | 14 | 0.9729 | A Sco homologue plays a role in defence against oxidative stress in pathogenic Neisseria. Sco proteins are found in mitochondria and in a variety of oxidase positive bacteria. Although Sco is required for the formation of the Cu(A) centre in a cytochrome oxidase of the aa(3) type, it was observed that oxidases with a Cu(A) centre are not present in many bacteria that contain a Sco homologue. Two bacteria of this type are the pathogens Neisseria meningitidis and Neisseria gonorrhoeae. The sco genes of N. gonorrhoeae strain 1291 and N. meningitidis strain MC58 were cloned, inactivated by inserting a kanamycin resistance cassette and used to make knockout mutants by allelic exchange. Both N. gonorrhoeae and N. meningitidis sco mutants were highly sensitive to oxidative killing by paraquat, indicating that Sco is involved in protection against oxidative stress in these bacteria. | 2003 | 12832079 |
| 60 | 15 | 0.9729 | Arabidopsis NHO1 is required for general resistance against Pseudomonas bacteria. Nonhost interactions are prevalent between plants and specialized phytopathogens. Although it has great potential for providing crop plants with durable resistance, nonhost resistance is poorly understood. Here, we show that nonhost resistance is controlled, at least in part, by general resistance. Arabidopsis plants are resistant to the nonhost pathogen Pseudomonas syringae pv phaseolicola NPS3121 and completely arrest bacterial multiplication in the plant. Ten Arabidopsis mutants were isolated that were compromised in nonhost (nho) resistance to P. s. phaseolicola. Among these, nho1 is caused by a single recessive mutation that defines a novel gene. nho1 is defective in nonspecific resistance to Pseudomonas bacteria, because it also supported the growth of P. s. tabaci and P. fluorescens bacteria, both of which are nonpathogenic on Arabidopsis. In addition, the nho1 mutation also compromised resistance mediated by RPS2, RPS4, RPS5, and RPM1. Interestingly, the nho1 mutation had no effect on the growth of the virulent bacteria P. s. maculicola ES4326 and P. s. tomato DC3000, but it partially restored the in planta growth of the DC3000 hrpS(-) mutant bacteria. Thus, the virulent bacteria appear to evade or suppress NHO1-mediated resistance by means of an Hrp-dependent virulence mechanism. | 2001 | 11226196 |
| 6178 | 16 | 0.9728 | Involvement of MarR and YedS in carbapenem resistance in a clinical isolate of Escherichia coli from China. A carbapenem-resistant clinical isolate of Escherichia coli, which lacked OmpF and OmpC porins, carried a marR mutation and expressed a functional yedS, a normally nontranslated gene. MarR and YedS are described here as having effects on the ability of this strain to resist carbapenems. Additionally, expression of YedS was regulated by the small RNA MicF in a MarA-dependent way. These findings illustrate how broadly bacteria can mutate within a selective clinical setting, in this case, resistance to carbapenems, by altering three porin genes and one regulatory gene. | 2013 | 23318808 |
| 393 | 17 | 0.9728 | Antibiotic marker modifications of lambda Red and FLP helper plasmids, pKD46 and pCP20, for inactivation of chromosomal genes using PCR products in multidrug-resistant strains. The Red recombinase system of bacteriophage Lambda has been used to inactivate chromosomal genes in bacteria using PCR products. In this study, we describe the replacement of the ampicillin resistance marker of helper plasmids pKD46 and pCP20 by a gentamicin resistance gene to disrupt chromosomal genes and then to eliminate FRT flanked resistance gene in multiple antibiotic-resistant Salmonella enterica strains. | 2008 | 18619499 |
| 3742 | 18 | 0.9728 | Lipophilic teicoplanin pseudoaglycon derivatives are active against vancomycin- and teicoplanin-resistant enterococci. A selection of nine derivatives of teicoplanin pseudoaglycon were tested in vitro against clinical vancomycin-resistant Enterococcus strains possessing vanA, vanB or both genes. The bacteria were characterized by PCR for the identification of their resistance genes. The tested compounds contain lipoic acid, different carbohydrates and aryl groups as lipophilic moieties. About one-third of the teicoplanin-resistant strains were shown to be susceptible to one or more of the glycopeptide derivatives. | 2017 | 28144040 |
| 8197 | 19 | 0.9728 | Specific host genes required for the killing of Klebsiella bacteria by phagocytes. The amoeba Dictyostelium discoideum shares many traits with mammalian macrophages, in particular the ability to phagocytose and kill bacteria. In response, pathogenic bacteria use conserved mechanisms to fight amoebae and mammalian phagocytes. Here we developed an assay using Dictyostelium to monitor phagocyte-bacteria interactions. Genetic analysis revealed that the virulence of Klebsiella pneumoniae measured by this test is very similar to that observed in a mouse pneumonia model. Using this assay, two new host resistance genes (PHG1 and KIL1) were identified and shown to be involved in intracellular killing of K. pneumoniae by phagocytes. Phg1 is a member of the 9TM family of proteins, and Kil1 is a sulphotransferase. The loss of PHG1 resulted in Dictyostelium susceptibility to a small subset of bacterial species including K. pneumoniae. Remarkably, Drosophila mutants deficient for PHG1 also exhibited a specific susceptibility to K. pneumoniae infections. Systematic analysis of several additional Dictyostelium mutants created a two-dimensional virulence array, where the complex interactions between host and bacteria are visualized. | 2006 | 16367873 |