# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 823 | 0 | 0.9769 | Characterization of the prtA and prtB genes of Erwinia chrysanthemi EC16. Two tandem metalloprotease-encoding structural genes, prtA and prtB, were sequenced from Erwinia chrysanthemi EC16. These were highly homologous to previously reported genes from the same bacteria, as well as to three other metalloprotease-encoding genes from enteric bacteria. The three tandem prt structural genes from strain EC16 were closely linked to a cluster of genes previously found to be essential for extracellular secretion of the metalloproteases. | 1993 | 8224883 |
| 460 | 1 | 0.9755 | Horizontal transfer of the photosynthesis gene cluster and operon rearrangement in purple bacteria. A 37-kb photosynthesis gene cluster was sequenced in a photosynthetic bacterium belonging to the beta subclass of purple bacteria (Proteobacteria), Rubrivivax gelatinosus. The cluster contained 12 bacteriochlorophyll biosynthesis genes (bch), 7 carotenoid biosynthesis genes (crt), structural genes for photosynthetic apparatuses (puf and puh), and some other related genes. The gene arrangement was markedly different from those of other purple photosynthetic bacteria, while two superoperonal structures, crtEF-bchCXYZ-puf and bchFNBHLM-lhaA-puhA, were conserved. Molecular phylogenetic analyses of these photosynthesis genes showed that the photosynthesis gene cluster of Rvi. gelatinosus was originated from those of the species belonging to the alpha subclass of purple bacteria. It was concluded that a horizontal transfer of the photosynthesis gene cluster from an ancestral species belonging to the alpha subclass to that of the beta subclass of purple bacteria had occurred and was followed by rearrangements of the operons in this cluster. | 2001 | 11343129 |
| 5222 | 2 | 0.9754 | Resistance to macrolides by ribosomal mutation in clinical isolates of Turicella otitidis. The genetic basis of erythromycin resistance in Turicella otitidis, a coryneform bacteria associated with otitis, was studied in five macrolide-resistant clinical isolates. Macrolide resistance genes were searched for by polymerase chain reaction (PCR). Genes for domain V of 23S rRNA (rrl) as well as rplD (L4 protein) and rplV (L22 protein) genes were characterised, amplified by PCR from total genomic DNA and sequenced. In the resistant isolates, cross-resistance to macrolides and clindamycin was associated with mutations at positions 2058 and/or 2059 (Escherichia coli numbering). Three isolates displayed A2058 mutations, one isolate had an A2059G mutation whereas another one contained mutations at positions 2058 and 2059. Southern blot experiments revealed that T. otitidis had three copies of the rrl gene. In conclusion, resistance to macrolides in T. otitidis is due, at least in part, to mutations in the rrl gene. | 2009 | 19414240 |
| 530 | 3 | 0.9752 | Location of the genes for anthranilate synthase in Streptomyces venezuelae ISP5230: genetic mapping after integration of the cloned genes. The anthranilate synthase (trpEG) genes in Streptomyces venezuelae ISP5230 were located by allowing a segregationally unstable plasmid carrying cloned S. venezuelae trpEG DNA and a thiostrepton resistance (tsr) marker to integrate into the chromosome. The integrated tsr was mapped by conjugation and transduction to a location close to tyr-2, between arg-6 and trpA13. A genomic DNA fragment containing trpC from S. venezuelae ISP5230 was cloned by complementation of a trpC mutation in Streptomyces lividans. Evidence from restriction enzyme analysis of the cloned DNA fragments, from Southern hybridization using the cloned trp DNA as probes, and from cotransduction frequencies, placed trpEG at a distance of 12-45 kb from the trpCBA cluster. The overall arrangement of tryptophan biosynthesis genes in the S. venezuelae chromosome differs from that in other bacteria examined so far. | 1993 | 8515229 |
| 351 | 4 | 0.9749 | Rapid and efficient cloning of proviral flanking fragments by kanamycin resistance gene complementation. We have developed a technique for the rapid cloning of unknown flanking regions of transgenic DNA. We complemented a truncated kanamycin resistance gene of a bacterial plasmid with a neomycin resistance gene fragment from a gene transfer vector. Optimized transformation conditions allowed us to directly select for kanamycin-resistant bacteria. We cloned numerous proviral flanking fragments from growth factor-independent cell mutants that were obtained after infection with a replication incompetent retroviral vector and identified integrations into the cyclin D2 and several unknown genomic sequences. We anticipate that our method could be adapted to various vector systems that are used to tag and identify genes and to map genomes. | 1999 | 9863001 |
| 575 | 5 | 0.9748 | 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 |
| 605 | 6 | 0.9746 | Conservation and diversity of the IrrE/DdrO-controlled radiation response in radiation-resistant Deinococcus bacteria. The extreme radiation resistance of Deinococcus bacteria requires the radiation-stimulated cleavage of protein DdrO by a specific metalloprotease called IrrE. DdrO is the repressor of a predicted radiation/desiccation response (RDR) regulon, composed of radiation-induced genes having a conserved DNA motif (RDRM) in their promoter regions. Here, we showed that addition of zinc ions to purified apo-IrrE, and short exposure of Deinococcus cells to zinc ions, resulted in cleavage of DdrO in vitro and in vivo, respectively. Binding of IrrE to RDRM-containing DNA or interaction of IrrE with DNA-bound DdrO was not observed. The data are in line with IrrE being a zinc peptidase, and indicate that increased zinc availability, caused by oxidative stress, triggers the in vivo cleavage of DdrO unbound to DNA. Transcriptomics and proteomics of Deinococcus deserti confirmed the IrrE-dependent regulation of predicted RDR regulon genes and also revealed additional members of this regulon. Comparative analysis showed that the RDR regulon is largely well conserved in Deinococcus species, but also showed diversity in the regulon composition. Notably, several RDR genes with an important role in radiation resistance in Deinococcus radiodurans, for example pprA, are not conserved in some other radiation-resistant Deinococcus species. | 2017 | 28397370 |
| 286 | 7 | 0.9746 | Plasmid rescue - a tool for reproducible recovery of genes from transfected mammalian cells? The efficient rescue of plasmids containing the thymidine kinase gene (tk) of Herpes simplex virus type I from genetically transformed mouse cells by transformation of bacteria is described. Rescued plasmids contain insertions of calf DNA used as a carrier in the transfection but usually lack portions of plasmid DNA. Deletions generally concern the region spanning from around the PvuII site of pBR322 to within the tetracycline resistance coding sequence, whereas the extent of tk sequence deletion varies, depending on the site of its integration (BamHI or PvuII) into the plasmid. Modelling the rescue process by transformation of bacteria with a mixture of original plasmids and sheared mouse cell DNA clearly demonstrates that deletions are caused by the presence of the mammalian DNA and they probably occur during re-transformation of bacteria before the onset of tetracycline gene expression. Plasmids lacking the Tcr region are reproducibly rescuable without deletion. Methods for reproducible re-isolation of transferred genes from mammalian cells are discussed. | 1984 | 6323922 |
| 6131 | 8 | 0.9743 | Draft Genome Sequence of Eggerthia catenaformis Strain MAR1 Isolated from Saliva of Healthy Humans. Here, we report the draft genome sequence of Eggerthia catenaformis MAR1 isolated during a screen for d-cycloserine-resistant bacteria from the saliva of healthy humans. Analysis of the genome reveals that the strain has the potential to be a human pathogen and carries genes related to virulence and antibiotic resistance. | 2017 | 28705984 |
| 396 | 9 | 0.9741 | A novel, highly efficient gene-cloning system in Micromonospora applied to the genetic analysis of fortimicin biosynthesis. We have developed a gene-cloning system in Micromonospora olivasterospora, a fortimicin A (astromicin) producer. Plasmids of Micromonospora from two strains of M. olivasterospora were used for construction of the vectors. Two antibiotic-resistance genes, nmrA and nmrB, cloned from a neomycin-producing Micromonospora, were introduced into these plasmids for the selection of transformants. In a new protoplasting protocol for lysozyme-resistant bacteria, protoplasts of M. olivasterospora were found in short-time incubation with lysozyme and transformed efficiently, indicating that the method was suitable to shotgun cloning. Using this system, seven biosynthetic genes for fortimicin A were cloned. Their physical maps revealed that at least four of these genes were clustered. Analysis of a cosmid library of M. olivasterospora showed that eleven biosynthetic genes and a self-defense gene existed in a region of approx. 25 kb of DNA. | 1992 | 1612453 |
| 9981 | 10 | 0.9740 | High-contrast imaging of cellular non-repetitive drug-resistant genes via in situ dead Cas12a-labeled PCR. In situ imaging of genes of pathogenic bacteria can profile cellular heterogeneity, such as the emergence of drug resistance. Fluorescence in situ hybridization (FISH) serves as a classic approach to image mRNAs inside cells, but it remains challenging to elucidate genomic DNAs and relies on multiple fluorescently labeled probes. Herein, we present a dead Cas12a (dCas12a)-labeled polymerase chain reaction (CasPCR) assay for high-contrast imaging of cellular drug-resistant genes. We employed a syncretic dCas12a-green fluorescent protein (dCas12a-GFP) to tag the amplicons, thereby enabling high-contrast imaging and avoiding multiple fluorescently labeled probes. The CasPCR assay can quantify quinolone-resistant Salmonella enterica in mixed populations and identify them isolated from poultry farms. | 2024 | 39229640 |
| 480 | 11 | 0.9739 | Permanent draft genome sequences of cadmium-resistant isolates of Cupriavidus from soils within the Tar Creek Superfund site. Soil samples taken near the abandoned town of Picher, OK, USA, were used to enrich and isolate bacteria in the presence of cadmium. Isolates reported belong to the genus Cupriavidus. Here, we report their permanent draft sequences with an emphasis on genes conferring resistance to cadmium. | 2025 | 39589146 |
| 573 | 12 | 0.9738 | Termination factor Rho and its cofactors NusA and NusG silence foreign DNA in E. coli. Transcription of the bacterial genome by the RNA polymerase must terminate at specific points. Transcription can be terminated by Rho factor, an essential protein in enterobacteria. We used the antibiotic bicyclomycin, which inhibits Rho, to assess its role on a genome-wide scale. Rho is revealed as a global regulator of gene expression that matches Escherichia coli transcription to translational needs. We also found that genes in E. coli that are most repressed by Rho are prophages and other horizontally acquired portions of the genome. Elimination of these foreign DNA elements increases resistance to bicyclomycin. Although rho remains essential, such reduced-genome bacteria no longer require Rho cofactors NusA and NusG. Deletion of the cryptic rac prophage in wild-type E. coli increases bicyclomycin resistance and permits deletion of nusG. Thus, Rho termination, supported by NusA and NusG, is required to suppress the toxic activity of foreign genes. | 2008 | 18487194 |
| 570 | 13 | 0.9738 | Genetic instability and methylation tolerance in colon cancer. Microsatellite instability was first identified in colon cancer and later shown to be due to mutations in genes responsible for correction of DNA mismatches. Several human mismatch correction genes that are homologous to those of yeast and bacteria have been identified and are mutated in families affected by the hereditary non-polyposis colorectal carcinoma (HNPCC) syndrome. Similar alterations have been also found in some sporadic colorectal cancers. The mismatch repair pathway corrects DNA replication errors and repair-defective colorectal carcinoma cell lines exhibit a generalized mutator phenotype. An additional consequence of mismatch repair defects is cellular resistance, or tolerance, to certain DNA damaging agents. | 1996 | 8967715 |
| 283 | 14 | 0.9736 | 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 |
| 105 | 15 | 0.9735 | 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 |
| 9991 | 16 | 0.9735 | A bifunctional dihydrofolate synthetase--folylpolyglutamate synthetase in Plasmodium falciparum identified by functional complementation in yeast and bacteria. Folate metabolism in the human malaria parasite Plasmodium falciparum is an essential activity for cell growth and replication, and the target of an important class of therapeutic agents in widespread use. However, resistance to antifolate drugs is a major health problem in the developing world. To date, only two activities in this complex pathway have been targeted by antimalarials. To more fully understand the mechanisms of antifolate resistance and to identify promising targets for new chemotherapies, we have cloned genes encoding as yet uncharacterised enzymes in this pathway. By means of complementation experiments using 1-carbon metabolism mutants of both Escherichia coli and Saccharomyces cerevisiae, we demonstrate here that one of these parasite genes encodes both dihydrofolate synthetase (DHFS) and folylpolyglutamate synthetase (FPGS) activities, which catalyse the synthesis and polyglutamation of folate derivatives, respectively. The malaria parasite is the first known example of a eukaryote encoding both DHFS and FPGS activities in a single gene. DNA sequencing of this gene in antifolate-resistant strains of P. falciparum, as well as drug-inhibition assays performed on yeast and bacteria expressing PfDHFS--FPGS, indicate that current antifolate regimes do not target this enzyme. As PfDHFS--FPGS harbours two activities critical to folate metabolism, one of which has no human counterpart, this gene product offers a novel chemotherapeutic target with the potential to deliver a powerful blockage to parasite growth. | 2001 | 11223131 |
| 112 | 17 | 0.9734 | Glycopeptide resistance determinants from the teicoplanin producer Actinoplanes teichomyceticus. In enterococci and other pathogenic bacteria, high-level resistance to vancomycin and other glycopeptide antibiotics requires the action of the van genes, which direct the synthesis of peptidoglycan terminating in the depsipeptide D-alanyl-D-lactate, in place of the usual D-Ala-D-Ala. The Actinoplanes teichomyceticus tcp cluster, devoted to the biosynthesis of the glycopeptide antibiotic teicoplanin, contains van genes associated to a murF-like sequence (murF2). We show that A. teichomyceticus contains also a house-keeping murF1 gene, capable of complementing a temperature sensitive Escherichia coli murF mutant. MurF1, expressed in Streptomyces lividans, can catalyze the addition of either D-Ala-D-Ala or D-Ala-D-Lac to the UDP-N-acetyl-muramyl-L-Ala-D-Glu-d-Lys. However, similarly expressed MurF2 shows a small enzymatic activity only with D-Ala-D-lactate. Introduction of a single copy of the entire set of van genes confers resistance to teicoplanin-type glycopeptides to S. coelicolor. | 2004 | 15500981 |
| 356 | 18 | 0.9734 | Development of an extrachromosomal cloning vector system for use in Borrelia burgdorferi. Molecular genetic analysis of Borrelia burgdorferi, the cause of Lyme disease, has been hampered by the absence of any means of efficient generation, identification, and complementation of chromosomal and plasmid null gene mutants. The similarity of borrelial G + C content to that of Gram-positive organisms suggested that a wide-host-range plasmid active in Gram-positive bacteria might also be recognized by borrelial DNA replication machinery. One such plasmid, pGK12, is able to propagate in both Gram-positive and Gram-negative bacteria and carries erythromycin and chloramphenicol resistance markers. pGK12 propagated extrachromosomally in B. burgdorferi B31 after electroporation but conferred only erythromycin resistance. pGK12 was used to express enhanced green fluorescent protein in B31 under the control of the flaB promoter. Escherichia coli transformed with pGK12 DNA extracted from B31 expressing only erythromycin resistance developed both erythromycin and chloramphenicol resistance, and plasmid DNA isolated from these transformed E. coli had a restriction pattern similar to the original pGK12. Our data indicate that the replicons of pGK12 can provide the basis to continue developing efficient genetic systems for B. burgdorferi together with the erythromycin resistance and reporter egfp genes. | 2000 | 10781091 |
| 479 | 19 | 0.9734 | Genome sequences of Methylobacterium and Methylorubrum isolates from Cd-contaminated soils in the Tar Creek Superfund site. Soil bacteria were isolated from the Tar Creek Superfund site in the presence of cadmium. Eight of these strains belong to the genus Methylobacterium, whereas one strain belongs to the genus Methylorubrum. Here, we report drafts of their genome sequences and highlight cadmium-resistance genes required in an exceptionally contaminated environment. | 2025 | 39835800 |