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Article ; Online: Recombination and DNA repair in Helicobacter pylori.

Dorer, Marion S / Sessler, Tate H / Salama, Nina R

2011 Volume 65, Page(s) 329–348

Abstract: All organisms have pathways that repair the genome, ensuring their survival and that of their progeny. But these pathways also serve to diversify the genome, causing changes at the nucleotide, whole gene, and genome structure levels. Sequencing of ... ...

Abstract	All organisms have pathways that repair the genome, ensuring their survival and that of their progeny. But these pathways also serve to diversify the genome, causing changes at the nucleotide, whole gene, and genome structure levels. Sequencing of bacteria has revealed wide allelic diversity and differences in gene content within the same species, highlighting the importance of understanding pathways of recombination and DNA repair. The human stomach pathogen Helicobacter pylori is an excellent model system for studying these pathways. H. pylori harbors major recombination and repair pathways and is naturally competent, facilitating its ability to diversify its genome. Elucidation of DNA recombination, repair, and diversification programs in this pathogen will reveal connections between these pathways and their importance to infection.
MeSH term(s)	Animals ; DNA Repair ; Helicobacter Infections/microbiology ; Helicobacter pylori/genetics ; Helicobacter pylori/physiology ; Humans ; Recombination, Genetic
Language	English
Publishing date	2011-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	207931-8
ISSN	1545-3251 ; 0066-4227
ISSN (online)	1545-3251
ISSN	0066-4227
DOI	10.1146/annurev-micro-090110-102931
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Article: Non-vertebrate hosts in the analysis of host-pathogen interactions.

Dorer, Marion S / Isberg, Ralph R

Microbes and infection

2006 Volume 8, Issue 6, Page(s) 1637–1646

Abstract: Mutations in bacterial pathogens have been isolated using many strategies. In contrast, the hosts they attack are significantly less tractable. To overcome this problem, a number of model host systems have been developed for isolation and investigation ... ...

Abstract	Mutations in bacterial pathogens have been isolated using many strategies. In contrast, the hosts they attack are significantly less tractable. To overcome this problem, a number of model host systems have been developed for isolation and investigation of mutations that modulate pathogen growth. These novel host models are either unicellular organisms, intact invertebrates or cells derived from invertebrates.
MeSH term(s)	Animals ; Bacteria/genetics ; Bacteria/growth & development ; Bacterial Infections/microbiology ; Caenorhabditis elegans/microbiology ; Caenorhabditis elegans/physiology ; Dictyostelium/microbiology ; Dictyostelium/physiology ; Drosophila melanogaster/microbiology ; Drosophila melanogaster/physiology ; Mutation
Language	English
Publishing date	2006-01-27
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	1465093-9
ISSN	1769-714X ; 1286-4579
ISSN (online)	1769-714X
ISSN	1286-4579
DOI	10.1016/j.micinf.2005.11.020
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Article ; Online: DNA damage triggers genetic exchange in Helicobacter pylori.

Dorer, Marion S / Fero, Jutta / Salama, Nina R

PLoS pathogens

2010 Volume 6, Issue 7, Page(s) e1001026

Abstract: Many organisms respond to DNA damage by inducing expression of DNA repair genes. We find that the human stomach pathogen Helicobacter pylori instead induces transcription and translation of natural competence genes, thus increasing transformation ... ...

Abstract	Many organisms respond to DNA damage by inducing expression of DNA repair genes. We find that the human stomach pathogen Helicobacter pylori instead induces transcription and translation of natural competence genes, thus increasing transformation frequency. Transcription of a lysozyme-like protein that promotes DNA donation from intact cells is also induced. Exogenous DNA modulates the DNA damage response, as both recA and the ability to take up DNA are required for full induction of the response. This feedback loop is active during stomach colonization, indicating a role in the pathogenesis of the bacterium. As patients can be infected with multiple genetically distinct clones of H. pylori, DNA damage induced genetic exchange may facilitate spread of antibiotic resistance and selection of fitter variants through re-assortment of preexisting alleles in this important human pathogen.
MeSH term(s)	DNA Damage ; Helicobacter pylori/genetics ; Helicobacter pylori/pathogenicity ; Humans ; Rec A Recombinases/genetics ; Transcription, Genetic ; Transformation, Genetic
Chemical Substances	Rec A Recombinases (EC 2.7.7.-)
Language	English
Publishing date	2010-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1001026
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Article ; Online: Characterization of Helicobacter pylori factors that control transformation frequency and integration length during inter-strain DNA recombination.

Humbert, Olivier / Dorer, Marion S / Salama, Nina R

Molecular microbiology

2010 Volume 79, Issue 2, Page(s) 387–401

Abstract: Helicobacter pylori is a genetically diverse bacterial species, owing in part to its natural competence for DNA uptake that facilitates recombination between strains. Inter-strain DNA recombination occurs during human infection and the H. pylori genome ... ...

Abstract	Helicobacter pylori is a genetically diverse bacterial species, owing in part to its natural competence for DNA uptake that facilitates recombination between strains. Inter-strain DNA recombination occurs during human infection and the H. pylori genome is in linkage equilibrium worldwide. Despite this high propensity for DNA exchange, little is known about the factors that limit the extent of recombination during natural transformation. Here, we identify restriction-modification (R-M) systems as a barrier to transformation with homeologous DNA and find that R-M systems and several components of the recombination machinery control integration length. Type II R-M systems, the nuclease nucT and resolvase ruvC reduced integration length whereas the helicase recG increased it. In addition, we characterized a new factor that promotes natural transformation in H. pylori, dprB. Although free recombination has been widely observed in H. pylori, our study suggests that this bacterium uses multiple systems to limit inter-strain recombination.
MeSH term(s)	Bacterial Proteins/metabolism ; DNA Helicases/metabolism ; DNA Restriction-Modification Enzymes ; DNA, Bacterial/genetics ; DNA, Bacterial/metabolism ; Deoxyribonucleases/metabolism ; Helicobacter pylori/genetics ; Recombinases/metabolism ; Recombination, Genetic ; Transformation, Bacterial
Chemical Substances	Bacterial Proteins ; DNA Restriction-Modification Enzymes ; DNA, Bacterial ; Recombinases ; Deoxyribonucleases (EC 3.1.-) ; DNA Helicases (EC 3.6.4.-)
Language	English
Publishing date	2010-11-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	619315-8
ISSN	1365-2958 ; 0950-382X
ISSN (online)	1365-2958
ISSN	0950-382X
DOI	10.1111/j.1365-2958.2010.07456.x
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Article ; Online: Helicobacter pylori's unconventional role in health and disease.

Dorer, Marion S / Talarico, Sarah / Salama, Nina R

PLoS pathogens

2009 Volume 5, Issue 10, Page(s) e1000544

Abstract: The discovery of a bacterium, Helicobacter pylori, that is resident in the human stomach and causes chronic disease (peptic ulcer and gastric cancer) was radical on many levels. Whereas the mouth and the colon were both known to host a large number of ... ...

Abstract	The discovery of a bacterium, Helicobacter pylori, that is resident in the human stomach and causes chronic disease (peptic ulcer and gastric cancer) was radical on many levels. Whereas the mouth and the colon were both known to host a large number of microorganisms, collectively referred to as the microbiome, the stomach was thought to be a virtual Sahara desert for microbes because of its high acidity. We now know that H. pylori is one of many species of bacteria that live in the stomach, although H. pylori seems to dominate this community. H. pylori does not behave as a classical bacterial pathogen: disease is not solely mediated by production of toxins, although certain H. pylori genes, including those that encode exotoxins, increase the risk of disease development. Instead, disease seems to result from a complex interaction between the bacterium, the host, and the environment. Furthermore, H. pylori was the first bacterium observed to behave as a carcinogen. The innate and adaptive immune defenses of the host, combined with factors in the environment of the stomach, apparently drive a continuously high rate of genomic variation in H. pylori. Studies of this genetic diversity in strains isolated from various locations across the globe show that H. pylori has coevolved with humans throughout our history. This long association has given rise not only to disease, but also to possible protective effects, particularly with respect to diseases of the esophagus. Given this complex relationship with human health, eradication of H. pylori in nonsymptomatic individuals may not be the best course of action. The story of H. pylori teaches us to look more deeply at our resident microbiome and the complexity of its interactions, both in this complex population and within our own tissues, to gain a better understanding of health and disease.
MeSH term(s)	Gastritis/microbiology ; Gastritis/physiopathology ; Helicobacter Infections/microbiology ; Helicobacter Infections/physiopathology ; Helicobacter pylori/physiology ; Humans ; Stomach/microbiology ; Stomach/physiology
Language	English
Publishing date	2009-10-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1000544
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Article ; Online: DNA damage triggers genetic exchange in Helicobacter pylori.

Marion S Dorer / Jutta Fero / Nina R Salama

PLoS Pathogens, Vol 6, Iss 7, p e

2010 Volume 1001026

Abstract	Many organisms respond to DNA damage by inducing expression of DNA repair genes. We find that the human stomach pathogen Helicobacter pylori instead induces transcription and translation of natural competence genes, thus increasing transformation frequency. Transcription of a lysozyme-like protein that promotes DNA donation from intact cells is also induced. Exogenous DNA modulates the DNA damage response, as both recA and the ability to take up DNA are required for full induction of the response. This feedback loop is active during stomach colonization, indicating a role in the pathogenesis of the bacterium. As patients can be infected with multiple genetically distinct clones of H. pylori, DNA damage induced genetic exchange may facilitate spread of antibiotic resistance and selection of fitter variants through re-assortment of preexisting alleles in this important human pathogen.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	612
Language	English
Publishing date	2010-07-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Aggravating genetic interactions allow a solution to redundancy in a bacterial pathogen.

O'Connor, Tamara J / Boyd, Dana / Dorer, Marion S / Isberg, Ralph R

Science (New York, N.Y.)

2012 Volume 338, Issue 6113, Page(s) 1440–1444

Abstract: Interactions between hosts and pathogens are complex, so understanding the events that govern these interactions requires the analysis of molecular mechanisms operating in both organisms. Many pathogens use multiple strategies to target a single event in ...

Abstract	Interactions between hosts and pathogens are complex, so understanding the events that govern these interactions requires the analysis of molecular mechanisms operating in both organisms. Many pathogens use multiple strategies to target a single event in the disease process, confounding the identification of the important determinants of virulence. We developed a genetic screening strategy called insertional mutagenesis and depletion (iMAD) that combines bacterial mutagenesis and RNA interference, to systematically dissect the interplay between a pathogen and its host. We used this technique to resolve the network of proteins secreted by the bacterium Legionella pneumophila to promote intracellular growth, a critical determinant of pathogenicity of this organism. This strategy is broadly applicable, allowing the dissection of any interface between two organisms involving numerous interactions.
MeSH term(s)	Animals ; Bacterial Proteins/genetics ; Bacterial Secretion Systems/genetics ; Cells, Cultured ; Drosophila melanogaster/cytology ; Flavoproteins/genetics ; Genetic Testing/methods ; Host-Pathogen Interactions/genetics ; Humans ; Legionella pneumophila/genetics ; Legionella pneumophila/growth & development ; Macrophages/microbiology ; Mutagenesis, Insertional/methods ; RNA Interference ; Sequence Deletion ; Vacuoles/physiology
Chemical Substances	Bacterial Proteins ; Bacterial Secretion Systems ; Flavoproteins ; SdhA protein, Bacteria
Language	English
Publishing date	2012-12-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.1229556
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Article: Characterization of Helicobacter pylori factors that control transformation frequency and integration length during inter-strain DNA recombination

Humbert, Olivier / Dorer, Marion S / Salama, Nina R

Molecular microbiology. 2011 Jan., v. 79, no. 2

2011

Abstract	Helicobacter pylori is a genetically diverse bacterial species, owing in part to its natural competence for DNA uptake that facilitates recombination between strains. Inter-strain DNA recombination occurs during human infection and the H. pylori genome is in linkage equilibrium worldwide. Despite this high propensity for DNA exchange, little is known about the factors that limit the extent of recombination during natural transformation. Here, we identify restriction-modification (R-M) systems as a barrier to transformation with homeologous DNA and find that R-M systems and several components of the recombination machinery control integration length. Type II R-M systems, the nuclease nucT and resolvase ruvC reduced integration length whereas the helicase recG increased it. In addition, we characterized a new factor that promotes natural transformation in H. pylori, dprB. Although free recombination has been widely observed in H. pylori, our study suggests that this bacterium uses multiple systems to limit inter-strain recombination.
Language	English
Dates of publication	2011-01
Size	p. 387-401.
Publishing place	Blackwell Publishing Ltd
Document type	Article
ZDB-ID	619315-8
ISSN	1365-2958 ; 0950-382X
ISSN (online)	1365-2958
ISSN	0950-382X
DOI	10.1111/j.1365-2958.2010.07456.x
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Article ; Online: Helicobacter pylori's unconventional role in health and disease.

Marion S Dorer / Sarah Talarico / Nina R Salama

PLoS Pathogens, Vol 5, Iss 10, p e

2009 Volume 1000544

Abstract	The discovery of a bacterium, Helicobacter pylori, that is resident in the human stomach and causes chronic disease (peptic ulcer and gastric cancer) was radical on many levels. Whereas the mouth and the colon were both known to host a large number of microorganisms, collectively referred to as the microbiome, the stomach was thought to be a virtual Sahara desert for microbes because of its high acidity. We now know that H. pylori is one of many species of bacteria that live in the stomach, although H. pylori seems to dominate this community. H. pylori does not behave as a classical bacterial pathogen: disease is not solely mediated by production of toxins, although certain H. pylori genes, including those that encode exotoxins, increase the risk of disease development. Instead, disease seems to result from a complex interaction between the bacterium, the host, and the environment. Furthermore, H. pylori was the first bacterium observed to behave as a carcinogen. The innate and adaptive immune defenses of the host, combined with factors in the environment of the stomach, apparently drive a continuously high rate of genomic variation in H. pylori. Studies of this genetic diversity in strains isolated from various locations across the globe show that H. pylori has coevolved with humans throughout our history. This long association has given rise not only to disease, but also to possible protective effects, particularly with respect to diseases of the esophagus. Given this complex relationship with human health, eradication of H. pylori in nonsymptomatic individuals may not be the best course of action. The story of H. pylori teaches us to look more deeply at our resident microbiome and the complexity of its interactions, both in this complex population and within our own tissues, to gain a better understanding of health and disease.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	630
Language	English
Publishing date	2009-10-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Natural competence promotes Helicobacter pylori chronic infection.

Dorer, Marion S / Cohen, Ilana E / Sessler, Tate H / Fero, Jutta / Salama, Nina R

Infection and immunity

2012 Volume 81, Issue 1, Page(s) 209–215

Abstract: Animal models are important tools for studies of human disease, but developing these models is a particular challenge with regard to organisms with restricted host ranges, such as the human stomach pathogen Helicobacter pylori. In most cases, H. pylori ... ...

Abstract	Animal models are important tools for studies of human disease, but developing these models is a particular challenge with regard to organisms with restricted host ranges, such as the human stomach pathogen Helicobacter pylori. In most cases, H. pylori infects the stomach for many decades before symptoms appear, distinguishing it from many bacterial pathogens that cause acute infection. To model chronic infection in the mouse, a human clinical isolate was selected for its ability to survive for 2 months in the mouse stomach, and the resulting strain, MSD132, colonized the mouse stomach for at least 28 weeks. During selection, the cagY component of the Cag type IV secretion system was mutated, disrupting a key interaction with host cells. Increases in both bacterial persistence and bacterial burden occurred prior to this mutation, and a mixed population of cagY(+) and cagY mutant cells was isolated from a single mouse, suggesting that mutations accumulate during selection and that factors in addition to the Cag apparatus are important for murine adaptation. Diversity in both alleles and genes is common in H. pylori strains, and natural competence mediates a high rate of interstrain genetic exchange. Mutations of the Com apparatus, a membrane DNA transporter, and DprA, a cytosolic competence factor, resulted in reduced persistence, although initial colonization was normal. Thus, exchange of DNA between genetically heterogeneous H. pylori strains may improve chronic colonization. The strains and methods described here will be important tools for defining both the spectrum of mutations that promote murine adaptation and the genetic program of chronic infection.
MeSH term(s)	Alleles ; Animals ; Bacterial Proteins/genetics ; Chronic Disease ; Disease Models, Animal ; Female ; Helicobacter Infections/genetics ; Helicobacter Infections/microbiology ; Helicobacter pylori/genetics ; Humans ; Mice ; Mice, Inbred C57BL ; Mutation ; Stomach/microbiology
Chemical Substances	Bacterial Proteins
Language	English
Publishing date	2012-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.01042-12
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