# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 6722 | 0 | 0.9839 | Studies on the bacterial permeability of non-woven fabrics and cotton fabrics. The permeability of cotton and non-woven fabrics to bacteria, air and water was studied. Non-woven fabrics, even when wet, showed low resistance to air, and high resistance to permeation of water and bacteria. Water-repellent cotton fabrics were resistant to permeation of water, air and bacteria, but these properties decreased on washing. Non-water-repellent cotton fabrics were poor bacterial barriers even when new. | 1986 | 2873172 |
| 9980 | 1 | 0.9838 | 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 |
| 8232 | 2 | 0.9830 | Small acid-soluble proteins with intrinsic disorder are required for UV resistance in Myxococcus xanthus spores. Bacterial sporulation in Gram-positive bacteria results in small acid-soluble proteins called SASPs that bind to DNA and prevent the damaging effects of UV radiation. Orthologs of Bacillus subtilis genes encoding SASPs can be found in many sporulating and nonsporulating bacteria, but they are noticeably absent from spore-forming, Gram-negative Myxococcus xanthus. This is despite the fact that M. xanthus can form UV-resistant spores. Here we report evidence that M. xanthus produces its own unique group of low-molecular-weight, acid-soluble proteins that facilitate UV resistance in spores. These M. xanthus-specific SASPs vary depending upon whether spore formation is induced by starvation inside cell aggregations of fruiting bodies or is induced artificially by glycerol induction. Molecular predictions indicate that M. xanthus SASPs may have some association with the cell walls of M. xanthus spores, which may signify a different mechanism of UV protection than that seen in Gram-positive spores. | 2011 | 21515768 |
| 9371 | 3 | 0.9825 | Coevolutionary history of predation constrains the evolvability of antibiotic resistance in prey bacteria. Understanding how the historical contingency of biotic interactions shapes the evolvability of bacterial populations is imperative for the predictability of the eco-evolutionary dynamics of microbial communities. While microbial predators like Myxococcus xanthus influence the frequency of antibiotic-resistant bacteria in nature, the effect of adaptation to the presence of predators on the evolvability of prey bacteria to future stressors is unclear. Hence, to understand the influence of the coevolutionary history of predation on the evolvability of antibiotic resistance, we propagated variants of E. coli, pre-adapted to distinct biotic and abiotic conditions, in gradually increasing concentrations of antibiotics. We show that pre-adaptation to predators limits the evolution of a high degree of antibiotic resistance. Moreover, lower degree of resistance in the evolved strains also incurs reduced fitness costs while preserving their ancestral ability to resist predation. Together, we demonstrate that the history of biotic interactions can strongly influence the evolvability of bacteria. | 2025 | 40461734 |
| 9316 | 4 | 0.9825 | Molecular basis of metronidazole resistance in pathogenic bacteria and protozoa. The molecular basis of metronidazole resistance has been examined in anaerobic bacteria, such as Bacteroides, Clostridium, and Helicobacter, and anaerobic parasitic protists such as Giardia, Entamoeba, and trichomonads. A variety of enzymatic and cellular alterations have been shown to correlate with metronidazole susceptibility in these pathogens; however, a common theme has been revealed. Resistant cells are typically deficient in drug activation. The frequent correlation between metronidazole resistance and ineffective drug activation suggests that drug resistance is the result of modification of proteins involved in drug activation. Copyright 1999 Harcourt Publishers Ltd. | 1999 | 11504503 |
| 558 | 5 | 0.9825 | Thiamine pyrophosphate riboswitches are targets for the antimicrobial compound pyrithiamine. Thiamine metabolism genes are regulated in numerous bacteria by a riboswitch class that binds the coenzyme thiamine pyrophosphate (TPP). We demonstrate that the antimicrobial action of the thiamine analog pyrithiamine (PT) is mediated by interaction with TPP riboswitches in bacteria and fungi. For example, pyrithiamine pyrophosphate (PTPP) binds the TPP riboswitch controlling the tenA operon in Bacillus subtilis. Expression of a TPP riboswitch-regulated reporter gene is reduced in transgenic B. subtilis or Escherichia coli when grown in the presence of thiamine or PT, while mutant riboswitches in these organisms are unresponsive to these ligands. Bacteria selected for PT resistance bear specific mutations that disrupt ligand binding to TPP riboswitches and derepress certain TPP metabolic genes. Our findings demonstrate that riboswitches can serve as antimicrobial drug targets and expand our understanding of thiamine metabolism in bacteria. | 2005 | 16356850 |
| 109 | 6 | 0.9823 | Identification of two putative ATP-cassette genes in Encephalitozoon intestinalis. Currently existing chemotherapeutic compounds are limited and few are effective for treating microsporidiosis. It is possible that resistance of Encephalitozoon to some drugs occurs by efflux mechanisms similar to those previously described for mammalian tumour cells, bacteria or protozoal parasites such as Plasmodium, Leishmania and Entamoeba histolytica. The data in the present study suggest that Encephalitozoon intestinalis contains at least one multidrug resistance gene. We report here two complete sequences EiABC1 and EiABC2, encoding different ATP-binding cassette genes from E. intestinalis, including a P-gp. | 2001 | 11730796 |
| 9195 | 7 | 0.9822 | Complement-resistance mechanisms of bacteria. Despite more than a century of parallel research on bacteria and the complement system, relatively little is known of the mechanisms whereby pathogenic bacteria can escape complement-related opsonophagocytosis and direct killing. It is likely that pathogenicity in bacteria has arisen more accidentally than in viruses, and on the basis of selection from natural mutants rather than by outright stealing or copying of genetic codes from the host. In this review we will discuss complement resistance as one of the features that makes a bacterium a pathogen. | 1999 | 10816084 |
| 105 | 8 | 0.9821 | Resistance of the cholera vaccine candidate IEM108 against CTXPhi infection. The cholera toxin (CT) genes ctxAB are carried on a lysogenic phage of Vibrio cholerae, CTXPhi, which can transfer ctxAB between toxigenic and nontoxigenic strains of bacteria. This transfer may pose a problem when live oral cholera vaccine is given to people in epidemic areas, because the toxin genes can be reacquired by the vaccine strains. To address this problem, we have constructed a live vaccine candidate, IEM108, which carries an El Tor-derived rstR gene. This gene encodes a repressor and can render bacterial resistance to CTXPhi infection. In this study, we evaluated the resistance of IEM108 against CTXPhi infection by using a CTXPhi marked for chloramphenicol (CAF) resistance and an in vivo model. We found that the cloned rstR gene rendered IEM108 immune to infection with the marked CTXPhi. In addition, the infection rate of IEM108 was even lower than that of the native CTXPhi-positive strain. These results suggest that the vaccine candidate IEM108 is resistant to infection by CTXPhi. | 2006 | 16343705 |
| 283 | 9 | 0.9821 | Inactivation of expression of several genes in a variety of bacterial species by EGS technology. The expression of gene products in bacteria can be inhibited by the use of RNA external guide sequences (EGSs) that hybridize to a target mRNA. Endogenous RNase P cleaves the mRNA in the complex, making it inactive. EGSs participate in this biochemical reaction as the data presented here show. They promote mRNA cleavage at the expected site and sometimes at other secondary sites. Higher-order structure must affect these reactions if the cleavage does not occur at the defined site, which has been determined by techniques based on their ability to find sites that are accessible to the EGS oligonucleotides. Sites defined by a random EGS technique occur as expected. Oligonucleotides made up primarily of defined or random nucleotides are extremely useful in inhibiting expression of the gyrA and rnpA genes from several different bacteria or the cat gene that determines resistance to chloramphenicol in Escherichia coli. An EGS made up of a peptide-phosphorodiamidate morpholino oligonucleotide (PPMO) does not cleave at the same site as an unmodified RNA EGS for reasons that are only partly understood. However, PPMO-EGSs are useful in inhibiting the expression of targeted genes from Gram-negative and Gram-positive organisms during ordinary growth in broth and may provide a basis for broad-spectrum antibiotics. | 2009 | 19416872 |
| 8353 | 10 | 0.9821 | Adaptive loss of tRNA gene expression leads to phage resistance in a marine Synechococcus cyanobacterium. Synechococcus is a significant primary producer in the oceans, coexisting with cyanophages, which are important agents of mortality. Bacterial resistance against phage infection is a topic of significant interest, yet little is known for ecologically relevant systems. Here we use exogenous gene expression and gene disruption to investigate mechanisms underlying intracellular resistance of marine Synechococcus WH5701 to the Syn9 cyanophage. The restriction-modification and Gabija defence systems possessed by Synechococcus WH5701 did not contribute to resistance. Instead, resistance was primarily driven by insufficient levels of Leu(TAA) tRNA, preventing translation of key phage genes in a passive, intracellular mode of resistance. Restoring cellular tRNA expression rendered the cyanobacterium sensitive to infection. We propose an evolutionary scenario whereby changes in cell codon usage, acquisition of tRNAs by the phage and loss of cell and phage tRNA expression resulted in an effective means of resistance, highlighting the dynamic interplay between bacteria and phages in shaping their co-evolutionary trajectories. | 2025 | 39753669 |
| 9369 | 11 | 0.9821 | Microfluidic Ecology Unravels the Genetic and Ecological Drivers of T4r Bacteriophage Resistance in E. coli: Insights into Biofilm-Mediated Evolution. We use a microfluidic ecology which generates non-uniform phage concentration gradients and micro-ecological niches to reveal the importance of time, spatial population structure and collective population dynamics in the de novo evolution of T4r bacteriophage resistant motile E. coli. An insensitive bacterial population against T4r phage occurs within 20 hours in small interconnected population niches created by a gradient of phage virions, driven by evolution in transient biofilm patches. Sequencing of the resistant bacteria reveals mutations at the receptor site of bacteriophage T4r as expected but also in genes associated with biofilm formation and surface adhesion, supporting the hypothesis that evolution within transient biofilms drives de novo phage resistance. | 2024 | 38826273 |
| 8238 | 12 | 0.9820 | Resistance to enediyne antitumor antibiotics by CalC self-sacrifice. Antibiotic self-resistance mechanisms, which include drug elimination, drug modification, target modification, and drug sequestration, contribute substantially to the growing problem of antibiotic resistance among pathogenic bacteria. Enediynes are among the most potent naturally occurring antibiotics, yet the mechanism of resistance to these toxins has remained a mystery. We characterize an enediyne self-resistance protein that reveals a self-sacrificing paradigm for resistance to highly reactive antibiotics, and thus another opportunity for nonpathogenic or pathogenic bacteria to evade extremely potent small molecules. | 2003 | 12970566 |
| 9412 | 13 | 0.9820 | Persistence: a copacetic and parsimonious hypothesis for the existence of non-inherited resistance to antibiotics. We postulate that phenotypic resistance to antibiotics, persistence, is not an evolved (selected-for) character but rather like mutation, an inadvertent product of different kinds of errors and glitches. The rate of generation of these errors is augmented by exposure to these drugs. The genes that have been identified as contributing to the production of persisters are analogous to the so-called mutator genes; they modulate the rate at which these errors occur and/or are corrected. In theory, these phenotypically resistant bacteria can retard the rate of microbiological cure by antibiotic treatment. | 2014 | 25090240 |
| 298 | 14 | 0.9820 | Molecular analysis of antibiotic tolerance in pneumococci. Widespread pneumococcal resistance and the emergence of tolerance underscores the need to develop new antimicrobials. Uncovering the mechanisms of autolysin activation could yield not only new antibacterial targets but also ways to eradicate a pool of bacteria facilitating the spread of resistance. Although several genes contributing to antibiotic tolerance among pneumococci have been identified, those important in the clinical arena thus far are in a single gene cluster, vex/pep27/vncS/vncR. Mutations within this signal transduction system represent at least one mechanism, which explains tolerance to both penicillin and vancomycin. Since mutations in this locus do not result in tolerance to penicillin alone, there must be other, yet unknown, mutations which account for tolerance to a single antibiotic. In the case of pneumococci, there exist two more autolysins other than LytA suggesting our understanding of how bacteria die is currently only at the beginning. | 2002 | 12195738 |
| 110 | 15 | 0.9820 | Resistance to the macrolide antibiotic tylosin is conferred by single methylations at 23S rRNA nucleotides G748 and A2058 acting in synergy. The macrolide antibiotic tylosin has been used extensively in veterinary medicine and exerts potent antimicrobial activity against Gram-positive bacteria. Tylosin-synthesizing strains of the Gram-positive bacterium Streptomyces fradiae protect themselves from their own product by differential expression of four resistance determinants, tlrA, tlrB, tlrC, and tlrD. The tlrB and tlrD genes encode methyltransferases that add single methyl groups at 23S rRNA nucleotides G748 and A2058, respectively. Here we show that methylation by neither TlrB nor TlrD is sufficient on its own to give tylosin resistance, and resistance is conferred by the G748 and A2058 methylations acting together in synergy. This synergistic mechanism of resistance is specific for the macrolides tylosin and mycinamycin that possess sugars extending from the 5- and 14-positions of the macrolactone ring and is not observed for macrolides, such as carbomycin, spiramycin, and erythromycin, that have different constellations of sugars. The manner in which the G748 and A2058 methylations coincide with the glycosylation patterns of tylosin and mycinamycin reflects unambiguously how these macrolides fit into their binding site within the bacterial 50S ribosomal subunit. | 2002 | 12417742 |
| 575 | 16 | 0.9820 | Identification and characterization of uvrA, a DNA repair gene of Deinococcus radiodurans. Deinococcus radiodurans is extraordinarily resistant to DNA damage, because of its unusually efficient DNA repair processes. The mtcA+ and mtcB+ genes of D. radiodurans, both implicated in excision repair, have been cloned and sequenced, showing that they are a single gene, highly homologous to the uvrA+ genes of other bacteria. The Escherichia coli uvrA+ gene was expressed in mtcA and mtcB strains, and it produced a high degree of complementation of the repair defect in these strains, suggesting that the UvrA protein of D. radiodurans is necessary but not sufficient to produce extreme DNA damage resistance. Upstream of the uvrA+ gene are two large open reading frames, both of which are directionally divergent from the uvrA+ gene. Evidence is presented that the proximal of these open reading frames may be irrB+. | 1996 | 8955293 |
| 9366 | 17 | 0.9819 | Impact of bacterial mutation rate on coevolutionary dynamics between bacteria and phages. Mutator bacteria are frequently found in natural populations of bacteria and although coevolution with parasitic viruses (phages) is thought to be one reason for their persistence, it remains unclear how the presence of mutators affects coevolutionary dynamics. We hypothesized that phages must themselves adapt more rapidly or go extinct, in the face of rapidly evolving mutator bacteria. We compared the coevolutionary dynamics of wild-type Pseudomonas fluorescens SBW25 with a lytic phage to the dynamics of an isogenic mutator of P. fluorescens SBW25 together with the same phage. At the beginning of the experiment both wild-type bacteria and mutator bacteria coevolved with phages. However, mutators rapidly evolved higher levels of sympatric resistance to phages. The phages were unable to "keep-up" with the mutator bacteria, and these rates of coevolution declined to less than the rates of coevolution between the phages and wild-type bacteria. By the end of the experiment, the sympatric resistance of the mutator bacteria was not significantly different to the sympatric resistance of the wild-type bacteria. This suggests that the importance of mutators in the coevolutionary interactions with a particular phage population is likely to be short-lived. More generally, the results demonstrate that coevolving enemies may escape from Red-Queen dynamics. | 2010 | 20497216 |
| 284 | 18 | 0.9819 | Expression of a transposable antibiotic resistance element in Saccharomyces. Some eukaryotic genes can be expressed in bacteria but there are few examples of the expression of prokaryotic genes in eukaryotes. Antibiotic G418 is a 2-deoxystreptamine antibiotic that is structurally related to gentamicin but has inhibitory activity against a much wider variety of pro- and eukaryotic organisms. In bacteria, resistance to G418 can be determined by several plasmid-encoded modifiying enzymes and, in view of the broad spectrum of activity of G418, we considered that this antibiotic might be useful as a selective agent for the introduction of these antibiotic resistance genes into a eukaryotic organism such as Saccharomyces cerevisiae. Additional impetus for these experiments came from the knowledge that certain of the G418-resistance determinants in bacteria are carried on transposable elements; a study of the properties of these elements in eukaryotes would be intriguing. | 1980 | 6253817 |
| 3756 | 19 | 0.9819 | Ecological antibiotic policy. Development of resistance to antibiotics is a major problem worldwide. The normal oropharyngeal flora, the intestinal flora and the skin flora play important roles in this development. Within a few days after the onset of antibiotic therapy, resistant Escherichia coli, Haemophilus influenzae and Staphylococcus epidermidis can be detected in the normal flora of volunteers or patients. Horizontal spread of the resistance genes to other species, e.g. Salmonella spp., Staphylococcus aureus and Streptococcus pneumoniae, occurs by conjugation or transformation. An ecologically sound antibiotic policy favours the use of antibiotics with little or no impact on the normal flora. Prodrug antibiotics which are not active against the bacteria in the mouth and the intestine (before absorption) and which are not excreted to a significant degree via the intestine, saliva or skin are therefore preferred. Prodrugs such as pivampicillin, bacampicillin, pivmecillinam and cefuroxime axetil are favourable from an ecological point of view. Experience from Scandinavia supports this, since resistance to mecillinam after 20 years of use is low (about 5%) and stable. | 2000 | 11051626 |