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  • 1
    Language: English
    In: Journal of bacteriology, March 2011, Vol.193(5), pp.1114-21
    Description: Natural transformation by competence is a major mechanism of horizontal gene transfer in bacteria. Competence is defined as the genetically programmed physiological state that enables bacteria to actively take up DNA from the environment. The conditions that signal competence development are multiple and elusive, complicating the understanding of its evolutionary significance. We used expression of the competence gene comEA as a reporter of competence development and screened several hundred molecules for their ability to induce competence in the freshwater living pathogen Legionella pneumophila. We found that comEA expression is induced by chronic exposure to genotoxic molecules such as mitomycin C and antibiotics of the fluoroquinolone family. These results indicated that, in L. pneumophila, competence may be a response to genotoxic stress. Sunlight-emitted UV light represents a major source of genotoxic stress in the environment and we found that exposure to UV radiation effectively induces competence development. For the first time, we show that genetic exchanges by natural transformation occur within an UV-stressed population. Genotoxic stress induces the RecA-dependent SOS response in many bacteria. However, genetic and phenotypic evidence suggest that L. pneumophila lacks a prototypic SOS response and competence development in response to genotoxic stress is RecA independent. Our results strengthen the hypothesis that competence may have evolved as a DNA damage response in SOS-deficient bacteria. This parasexual response to DNA damage may have enabled L. pneumophila to acquire and propagate foreign genes, contributing to the emergence of this human pathogen.
    Keywords: Ultraviolet Rays ; Anti-Bacterial Agents -- Pharmacology ; Legionella Pneumophila -- Drug Effects
    ISSN: 00219193
    E-ISSN: 1098-5530
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  • 2
    Language: English
    In: Current Opinion in Microbiology, October 2012, Vol.15(5), pp.570-576
    Description: ► SOS-inducing antibiotics induce natural competence in non-SOS bacterial species. ► Competence regulatory circuits are diverse, yet they are induced by antibiotics. ► SOS substitution by competence could thus be common among bacterial pathogens. ► Natural transformation promotes genetic diversification in some species. ► Antibiotics could thus accelerate evolution of virulence in transformable species. Bacterial transformation is a programmed process resulting in genetic transfer and diversity. It relies on the development of competence via regulatory circuits which are diverse and tailored to the particular lifestyle of each species. Despite this diversity, some species have been reported to trigger competence in response to antibiotics. Here, we review these recent findings, which reinforce the view that competence is a stress response and can substitute for SOS in bacteria lacking it.
    Keywords: Biology
    ISSN: 1369-5274
    E-ISSN: 1879-0364
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  • 3
    Language: English
    In: The Journal of Bacteriology, 2011, Vol. 193(5), p.1114
    ISSN: 0021-9193
    ISSN: 00219193
    Source: American Society of Microbiology
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  • 4
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 02 August 2016, Vol.113(31), pp.8813-8
    Description: A highly conserved DNA uptake system allows many bacteria to actively import and integrate exogenous DNA. This process, called natural transformation, represents a major mechanism of horizontal gene transfer (HGT) involved in the acquisition of virulence and antibiotic resistance determinants. Despite evidence of HGT and the high level of conservation of the genes coding the DNA uptake system, most bacterial species appear non-transformable under laboratory conditions. In naturally transformable species, the DNA uptake system is only expressed when bacteria enter a physiological state called competence, which develops under specific conditions. Here, we investigated the mechanism that controls expression of the DNA uptake system in the human pathogen Legionella pneumophila We found that a repressor of this system displays a conserved ProQ/FinO domain and interacts with a newly characterized trans-acting sRNA, RocR. Together, they target mRNAs of the genes coding the DNA uptake system to control natural transformation. This RNA-based silencing represents a previously unknown regulatory means to control this major mechanism of HGT. Importantly, these findings also show that chromosome-encoded ProQ/FinO domain-containing proteins can assist trans-acting sRNAs and that this class of RNA chaperones could play key roles in post-transcriptional gene regulation throughout bacterial species.
    Keywords: Legionella Pneumophila ; Proq/Fino ; RNA Chaperone ; Natural Transformation ; Non-Coding RNA ; Gene Expression Regulation, Bacterial ; Gene Transfer, Horizontal ; Legionella Pneumophila -- Genetics ; RNA, Bacterial -- Genetics
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 5
    Language: English
    In: Journal of Bacteriology, August, 2004, Vol.186(15-16), p.5486(10)
    Description: Enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC) strains are human and animal pathogens that inject effector proteins into host cells via a type III secretion system (TTSS). Cif is an effector protein which induces host cell cycle arrest and reorganization of the actin cytoskeleton. Cif is encoded by a lambdoid prophage present in most of the EPEC and EHEC strains. In this study, we analyzed the domain that targets Cif to the TTSS by using a new reporter system based on a translational fusion of the effector proteins with mature TEM-1 [beta]-lactamase. Translocation was detected directly in living host cells by using the fluorescent [beta]-lactamase substrate CCF2/AM. We show that the first 16 amino acids (aa) of Cif were necessary and sufficient to mediate translocation into the host cells. Similarly, the first 20 aa of the effector proteins Map, EspF, and Tir, which are encoded in the same region as the TTSS, mediated secretion and translocation in a type III-dependent but chaperone-independent manner. A truncated form of Cif lacking its first 20 aa was no longer secreted and translocated, but fusion with the first 20 aa of Tir, Map, or EspF restored both secretion and translocation. In addition, the chimeric proteins were fully able to trigger host cell cycle arrest and stress fiber formation. In conclusion, our results demonstrate that Cif is composed of a C-terminal effector domain and an exchangeable N-terminal translocation signal and that the TEM-1 reporter system is a convenient tool for the study of the translocation of toxins or effector proteins into host cells.
    Keywords: Escherichia Coli -- Research ; Pathogenic Microorganisms -- Research
    ISSN: 0021-9193
    Source: Cengage Learning, Inc.
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  • 6
    Language: English
    In: Antimicrobial agents and chemotherapy, February 2018, Vol.62(2)
    Description: -Translation is a ribosome-rescue system that is ubiquitous in bacteria. Small molecules defining a new family of oxadiazole compounds that inhibit -translation have been found to have broad-spectrum antibiotic activity. We sought to determine the activity of KKL-35, a potent member of the oxadiazole family, against the human pathogen and other related species that can also cause Legionnaires' disease (LD). Consistent with the essential nature of -translation in , KKL-35 inhibited the growth of all tested strains at submicromolar concentrations. KKL-35 was also active against other LD-causing species. KKL-35 remained equally active against mutants that have evolved resistance to macrolides. KKL-35 inhibited the multiplication of in human macrophages at several stages of infection. No resistant mutants could be obtained, even during extended and chronic exposure. Surprisingly, KKL-35 was not synergistic with other ribosome-targeting antibiotics and did not induce the filamentation phenotype observed in cells defective for -translation. Importantly, KKL-35 remained active against mutants expressing an alternate ribosome-rescue system and lacking transfer-messenger RNA, the essential component of -translation. These results indicate that the antibiotic activity of KKL-35 is not related to the specific inhibition of -translation and its mode of action remains to be identified. In conclusion, KKL-35 is an effective antibacterial agent against the intracellular pathogen with no detectable resistance development. However, further studies are needed to better understand its mechanism of action and to assess further the potential of oxadiazoles in treatment.
    Keywords: Legionella ; Trans-Translation ; Anti-Bacterial Agents -- Pharmacology ; Benzamides -- Pharmacology ; Drug Resistance, Bacterial -- Drug Effects ; Legionella -- Drug Effects ; Legionella Pneumophila -- Drug Effects ; Oxadiazoles -- Pharmacology
    ISSN: 00664804
    E-ISSN: 1098-6596
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  • 7
    Language: English
    In: Journal of bacteriology, September 2010, Vol.192(17), pp.4504-16
    Description: Legionella pneumophila is an intracellular pathogen that infects protozoa in aquatic environments and when inhaled by susceptible human hosts replicates in alveolar macrophages and can result in the often fatal pneumonia called Legionnaires' disease. The ability of L. pneumophila to replicate within host cells requires the establishment of a specialized compartment that evades normal phagolysosome fusion called the Legionella-containing vacuole (LCV). Elucidation of the biochemical composition of the LCV and the identification of the regulatory signals sensed during intracellular replication are inherently challenging. L-Arginine is a critical nutrient in the metabolism of both prokaryotic and eukaryotic organisms. We showed that the L. pneumophila arginine repressor homolog, ArgR, is required for maximal intracellular growth in the unicellular host Acanthamoeba castellanii. In this study, we present evidence that the concentration of L-arginine in the LCV is sensed by ArgR to produce an intracellular transcriptional response. We characterized the L. pneumophila ArgR regulon by global gene expression analysis, identified genes highly affected by ArgR, showed that ArgR repression is dependent upon the presence of L-arginine, and demonstrated that ArgR-regulated genes are derepressed during intracellular growth. Additional targets of ArgR that may account for the argR mutant's intracellular multiplication defect are discussed. These results suggest that L-arginine availability functions as a regulatory signal during Legionella intracellular growth.
    Keywords: Arginine ; Gene Expression Regulation, Bacterial ; Legionella Pneumophila ; Bacterial Proteins -- Metabolism ; Repressor Proteins -- Metabolism ; Vacuoles -- Microbiology
    ISSN: 00219193
    E-ISSN: 1098-5530
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  • 8
    Language: English
    In: Journal of bacteriology, 01 October 2018, Vol.200(19)
    Description: is a nosocomial agent with a high propensity for developing resistance to antibiotics. This ability relies on horizontal gene transfer mechanisms occurring in the genus, including natural transformation. To study natural transformation in bacteria, the most prevalent method uses selection for the acquisition of an antibiotic resistance marker in a target chromosomal locus by the recipient cell. Most clinical isolates of are resistant to multiple antibiotics, limiting the use of such selection-based methods. Here, we report the development of a phenotypic and selection-free method based on flow cytometry to detect transformation events in multidrug-resistant (MDR) clinical isolates. To this end, we engineered a translational fusion between the abundant and conserved nucleoprotein (HU) and the superfolder green fluorescent protein (sfGFP). The new method was benchmarked against the conventional antibiotic selection-based method. Using this new method, we investigated several parameters affecting transformation efficiencies and identified conditions of transformability one hundred times higher than those previously reported. Using optimized transformation conditions, we probed natural transformation in a set of MDR clinical and nonclinical animal isolates. Regardless of their origin, the majority of the isolates displayed natural transformability, indicative of a conserved trait in the species. Overall, this new method and optimized protocol will greatly facilitate the study of natural transformation in the opportunistic pathogen Antibiotic resistance is a pressing global health concern with the rise of multiple and panresistant pathogens. The rapid and unfailing resistance to multiple antibiotics of the nosocomial agent , notably to carbapenems, prompt to understand the mechanisms behind acquisition of new antibiotic resistance genes. Natural transformation, one of the horizontal gene transfer mechanisms in bacteria, was only recently described in and could explain its ability to acquire resistance genes. We developed a reliable method to probe and study natural transformation mechanism in More broadly, this new method based on flow cytometry will allow experimental detection and quantification of horizontal gene transfer events in multidrug-resistant .
    Keywords: Acinetobacter Baumannii ; Acinetobacter ; Cytometry ; Horizontal Gene Transfer ; Natural Transformation ; Drug Resistance, Multiple, Bacterial ; Gene Transfer, Horizontal ; Transformation, Bacterial ; Acinetobacter Baumannii -- Genetics ; Anti-Bacterial Agents -- Pharmacology
    ISSN: 00219193
    E-ISSN: 1098-5530
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  • 9
    Language: English
    In: Journal of Bacteriology, Dec, 2008, Vol.190(23-24), p.8126(11)
    Description: RNase R is a processive 3'-5' exoribonuclease with a high degree of conservation in prokaryotes. Although some bacteria possess additional hydrolytic 3'-5' exoribonucleases such as RNase II, RNase R was found to be the only predicted one in the facultative intracellular pathogen Legionella pneumophila. This provided a unique opportunity to study the role of RNase R in the absence of an additional RNase with similar enzymatic activity. We investigated the role of RNase R in the biology of Legionella pneumophila under various conditions and performed gene expression profiling using microarrays. At optimal growth temperature, the loss of RNase R had no major consequence on bacterial growth and had a moderate impact on normal gene regulation. However, at a lower temperature, the loss of RNase R had a significant impact on bacterial growth and resulted in the accumulation of structured RNA degradation products. Concurrently, gene regulation was affected and specifically resulted in an increased expression of the competence regulon. Loss of the exoribonuclease activity of RNase R was sufficient to induce competence development, a genetically programmed process normally triggered as a response to environmental stimuli. The temperature-dependent expression of competence genes in the rnr mutant was found to be independent of previously identified competence regulators in Legionella pneumophila. We suggest that a physiological role of RNase R is to eliminate structured RNA molecules that are stabilized by low temperature, which in turn may affect regulatory networks, compromising adaptation to cold and thus resulting in decreased viability.
    Keywords: Ribonuclease -- Physiological Aspects ; Legionella Pneumophila -- Physiological Aspects ; Legionella Pneumophila -- Genetic Aspects
    ISSN: 0021-9193
    Source: Cengage Learning, Inc.
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  • 10
    Language: English
    In: Infection and Immunity, 2011, Vol. 79(5), p.1936
    Description: Legionella pneumophila is the etiological agent of Legionnaires' disease. Crucial to the pathogenesis of this intracellular pathogen is its ability to subvert host cell defenses, permitting intracellular replication in specialized vacuoles within host cells. The Dot/Icm type IV secretion system (T4SS), which translocates a large number of bacterial effectors into host cell, is absolutely required for rerouting the Legionella phagosome. Many Legionella effectors display distinctive eukaryotic domains, among which are protein kinase domains. In silico analysis and in vitro phosphorylation assays identified five functional protein kinases, LegK1 to LegK5, encoded by the epidemic L. pneumophila Lens strain. Except for LegK5, the Legionella protein kinases are all T4SS effectors. LegK2 plays a key role in bacterial virulence, as demonstrated by gene inactivation. The legK2 mutant containing vacuoles displays less-efficient recruitment of endoplasmic reticulum markers, which results in delayed intracellular replication. Considering that a kinase-dead substitution mutant of legK2 exhibits the same virulence defects, we highlight here a new molecular mechanism, namely, protein phosphorylation, developed by L. pneumophila to establish a replicative niche and evade host cell defenses. ; p. 1936-1950.
    Keywords: Legionella Pneumophila ; Protein Phosphorylation ; Secretion ; Vacuoles ; Genes ; Endoplasmic Reticulum ; Virulence ; Pathogenesis ; Protein Kinases ; Pathogens ; Mutants;
    ISSN: 0019-9567
    ISSN: 00199567
    E-ISSN: 10985522
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