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  • 1.
    Andersson, Dan I.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Hughes, Diarmaid
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Mikrobiologi.
    Antibiotic resistance and its cost: is it possible to reverse resistance?2010Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 8, nr 4, s. 260-271Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Most antibiotic resistance mechanisms are associated with a fitness cost that is typically observed as a reduced bacterial growth rate. The magnitude of this cost is the main biological parameter that influences the rate of development of resistance, the stability of the resistance and the rate at which the resistance might decrease if antibiotic use were reduced. These findings suggest that the fitness costs of resistance will allow susceptible bacteria to outcompete resistant bacteria if the selective pressure from antibiotics is reduced. Unfortunately, the available data suggest that the rate of reversibility will be slow at the community level. Here, we review the factors that influence the fitness costs of antibiotic resistance, the ways by which bacteria can reduce these costs and the possibility of exploiting them.

  • 2.
    Andersson, Dan I.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Hughes, Diarmaid
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Microbiological effects of sublethal levels of antibiotics2014Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 12, nr 7, s. 465-478Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The widespread use of antibiotics results in the generation of antibiotic concentration gradients in humans, livestock and the environment. Thus, bacteria are frequently exposed to non-lethal (that is, subinhibitory) concentrations of drugs, and recent evidence suggests that this is likely to have an important role in the evolution of antibiotic resistance. In this Review, we discuss the ecology of antibiotics and the ability of subinhibitory concentrations to select for bacterial resistance. We also consider the effects of low-level drug exposure on bacterial physiology, including the generation of genetic and phenotypic variability, as well as the ability of antibiotics to function as signalling molecules. Together, these effects accelerate the emergence and spread of antibiotic-resistant bacteria among humans and animals.

  • 3.
    Andersson, Dan I
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Nicoloff, Hervé
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Hjort, Karin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Mechanisms and clinical relevance of bacterial heteroresistance2019Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 17, nr 8, s. 479-496Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Antibiotic heteroresistance is a phenotype in which a bacterial isolate contains subpopulations of cells that show a substantial reduction in antibiotic susceptibility compared with the main population. Recent work indicates that heteroresistance is very common for several different bacterial species and antibiotic classes. The resistance phenotype is often unstable, and in the absence of antibiotic pressure it rapidly reverts to susceptibility. A common mechanistic explanation for the instability is the occurrence of genetically unstable tandem amplifications of genes that cause resistance. Due to their instability, low frequency and transient character, it is challenging to detect and study these subpopulations, which often leads to difficulties in unambiguously classifying bacteria as susceptible or resistant. Finally, in vitro experiments, mathematical modelling, animal infection models and clinical studies show that the resistant subpopulations can be enriched during antibiotic exposure, and increasing evidence suggests that heteroresistance can lead to treatment failure.

  • 4.
    Ankarklev, Johan
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Mikrobiologi.
    Jerlström-Hultqvist, Jon
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Mikrobiologi.
    Ringqvist, Emma
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Mikrobiologi.
    Troell, Karin
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Mikrobiologi.
    Svärd, Staffan G.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Mikrobiologi.
    Behind the smile: cell biology and disease mechanisms of Giardia species2010Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 8, nr 6, s. 413-422Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The eukaryotic intestinal parasite Giardia intestinalis was first described in 1681, when Antonie van Leeuwenhoek undertook a microscopic examination of his own diarrhoeal stool. Nowadays, although G. intestinalis is recognized as a major worldwide contributor to diarrhoeal disease in humans and other mammals, the disease mechanisms are still poorly understood. Owing to its reduced complexity and proposed early evolutionary divergence, G. intestinalis is used as a model eukaryotic system for studying many basic cellular processes. In this Review we discuss recent discoveries in the molecular cell biology and pathogenesis of G. intestinalis.

  • 5.
    Balaban, Nathalie Q.
    et al.
    Hebrew Univ Jerusalem, Racah Inst Phys, Jerusalem, Israel.
    Helaine, Sophie
    Imperial Coll London, MRC Ctr Mol Bacteriol & Infect, London, England.
    Lewis, Kim
    Northeastern Univ, Dept Biol, Boston, MA 02115 USA.
    Ackermann, Martin
    Swiss Fed Inst Technol, Inst Biogeochem & Pollutant Dynam, Zurich, Switzerland;Eawag, Dept Environm Microbiol, Dubendorf, Switzerland.
    Aldridge, Bree
    Tufts Univ, Sch Med, Dept Mol Biol & Microbiol, Boston, MA 02111 USA.
    Andersson, Dan I
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Brynildsen, Mark P.
    Princeton Univ, Dept Chem & Biol Engn, Princeton, NJ 08544 USA.
    Bumann, Dirk
    Univ Basel, Biozentrum, Focal Area Infect Biol, Basel, Switzerland.
    Camilli, Andrew
    Tufts Univ, Sch Med, Dept Mol Biol & Microbiol, Boston, MA 02111 USA.
    Collins, James J.
    MIT, Dept Biol Engn, Inst Med Engn & Sci, 77 Massachusetts Ave, Cambridge, MA 02139 USA;MIT, Synthet Biol Ctr, 77 Massachusetts Ave, Cambridge, MA 02139 USA;Harvard Univ, Wyss Inst Biol Inspired Engn, Boston, MA 02115 USA;Broad Inst MIT & Harvard, Cambridge, MA USA.
    Dehio, Christoph
    Univ Basel, Biozentrum, Focal Area Infect Biol, Basel, Switzerland.
    Fortune, Sarah
    Harvard TH Chan Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA USA.
    Ghigo, Jean-Marc
    Inst Pasteur, Genet Biofilms Lab, Paris, France.
    Hardt, Wolf-Dietrich
    Swiss Fed Inst Technol, Inst Microbiol, Zurich, Switzerland.
    Harms, Alexander
    Univ Basel, Biozentrum, Focal Area Infect Biol, Basel, Switzerland.
    Heinemann, Matthias
    Univ Groningen, Groningen Biomol Sci & Biotechnol Inst, Mol Syst Biol, Groningen, Netherlands.
    Hung, Deborah T.
    Broad Inst MIT & Harvard, Cambridge, MA USA.
    Jenal, Urs
    Univ Basel, Biozentrum, Focal Area Infect Biol, Basel, Switzerland.
    Levin, Bruce R.
    Emory Univ, Dept Biol, Atlanta, GA 30322 USA.
    Michiels, Jan
    Univ Leuven, KU Leuven, Ctr Microbiol, Leuven, Belgium.
    Storz, Gisela
    Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Mol & Cellular Biol, Bethesda, MD USA.
    Tan, Man-Wah
    Genentech Inc, Infect Dis Dept, San Francisco, CA USA.
    Tenson, Tanel
    Univ Tartu, Inst Technol, Tartu, Estonia.
    Van Melderen, Laurence
    Univ Libre Bruxelles, Fac Sci, Brussels, Belgium.
    Zinkernagel, Annelies
    Univ Zurich, Univ Hosp Zurich, Div Infect Dis, Zurich, Switzerland.
    Definitions and guidelines for research on antibiotic persistence2019Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 17, nr 7, s. 441-448Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Increasing concerns about the rising rates of antibiotic therapy failure and advances in single-cell analyses have inspired a surge of research into antibiotic persistence. Bacterial persister cells represent a subpopulation of cells that can survive intensive antibiotic treatment without being resistant. Several approaches have emerged to define and measure persistence, and it is now time to agree on the basic definition of persistence and its relation to the other mechanisms by which bacteria survive exposure to bactericidal antibiotic treatments, such as antibiotic resistance, heteroresistance or tolerance. In this Consensus Statement, we provide definitions of persistence phenomena, distinguish between triggered and spontaneous persistence and provide a guide to measuring persistence. Antibiotic persistence is not only an interesting example of non-genetic single-cell heterogeneity, it may also have a role in the failure of antibiotic treatments. Therefore, it is our hope that the guidelines outlined in this article will pave the way for better characterization of antibiotic persistence and for understanding its relevance to clinical outcomes.

  • 6. Batut, Jacques
    et al.
    Andersson, Siv
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för evolution, genomik och systematik, Molekylär evolution.
    O'Callaghan, David
    The evolution of chronic infection strategies in the α-proteobacteria2004Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 2, s. 933-945Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Many of the -proteobacteria establish long-term, often chronic, interactions with higher eukaryotes. These interactions range from pericellular colonization through facultative intracellular multiplication to obligate intracellular lifestyles. A common feature in this wide range of interactions is modulation of host-cell proliferation, which sometimes leads to the formation of tumour-like structures in which the bacteria can grow. Comparative genome analyses reveal genome reduction by gene loss in the intracellular -proteobacterial lineages, and genome expansion by gene duplication and horizontal gene transfer in the free-living species. In this review, we discuss -proteobacterial genome evolution and highlight strategies and mechanisms used by these bacteria to infect and multiply in eukaryotic cells.

  • 7.
    Eme, Laura
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Spang, Anja
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Lombard, Jonathan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Stairs, Courtney W
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Ettema, Thijs J G
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Archaea and the origin of eukaryotes.2018Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 16, nr 2, artikel-id 120Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    This corrects the article DOI: 10.1038/nrmicro.2017.133.

  • 8.
    Eme, Laura
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Molekylär evolution. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Spang, Anja
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Molekylär evolution. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Lombard, Jonathan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Molekylär evolution. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Stairs, Courtney W.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Molekylär evolution. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Ettema, Thijs J. G.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Molekylär evolution. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Archaea and the origin of eukaryotes2017Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 15, nr 12, s. 711-723Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Woese and Fox's 1977 paper on the discovery of the Archaea triggered a revolution in the field of evolutionary biology by showing that life was divided into not only prokaryotes and eukaryotes. Rather, they revealed that prokaryotes comprise two distinct types of organisms, the Bacteria and the Archaea. In subsequent years, molecular phylogenetic analyses indicated that eukaryotes and the Archaea represent sister groups in the tree of life. During the genomic era, it became evident that eukaryotic cells possess a mixture of archaeal and bacterial features in addition to eukaryotic-specific features. Although it has been generally accepted for some time that mitochondria descend from endosymbiotic alphaproteobacteria, the precise evolutionary relationship between eukaryotes and archaea has continued to be a subject of debate. In this Review, we outline a brief history of the changing shape of the tree of life and examine how the recent discovery of a myriad of diverse archaeal lineages has changed our understanding of the evolutionary relationships between the three domains of life and the origin of eukaryotes. Furthermore, we revisit central questions regarding the process of eukaryogenesis and discuss what can currently be inferred about the evolutionary transition from the first to the last eukaryotic common ancestor.

  • 9.
    Holmqvist, Erik
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Mikrobiologi.
    Vogel, Jörg
    Helmholtz Inst RNA Based Infect Res HIRI, Wurzburg, Germany;Univ Wurzburg, Inst Mol Infect Biol, Wurzburg, Germany.
    RNA-binding proteins in bacteria2018Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 16, nr 10, s. 601-615Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    RNA-binding proteins (RBPs) are central to most if not all cellular processes, dictating the fate of virtually all RNA molecules in the cell. Starting with pioneering work on ribosomal proteins, studies of bacterial RBPs have paved the way for molecular studies of RNA-protein interactions. Work over the years has identified major RBPs that act on cellular transcripts at the various stages of bacterial gene expression and that enable their integration into post-transcriptional networks that also comprise small non-coding RNAs. Bacterial RBP research has now entered a new era in which RNA sequencing-based methods permit mapping of RBP activity in a truly global manner in vivo. Moreover, the soaring interest in understudied members of host-associated microbiota and environmental communities is likely to unveil new RBPs and to greatly expand our knowledge of RNA-protein interactions in bacteria.

  • 10. Johansson, Cecilia
    et al.
    Schwartz, Stefan
    Regulation of human papillomavirus gene expression by splicing and polyadenylation.2013Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 11, nr 4, s. 239-51Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Human papillomaviruses (HPVs) are small DNA tumour viruses that are present in more than 99% of all cervical cancers. The ability of these viruses to cause disease is partly attributed to the strict coordination of viral gene expression with the differentiation stage of the infected cell. HPV gene expression is regulated temporally at the level of RNA splicing and polyadenylation, and a dysregulated gene expression programme allows some HPV types to establish long-term persistence, which is a risk factor for cancer. In this Review, we summarize the role of splicing and polyadenylation in the regulation of HPV gene expression and discuss the viral and cellular factors that control these processes.

  • 11. Martínez, José L.
    et al.
    Baquero, Fernando
    Andersson, Dan I.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Predicting antibiotic resistance2007Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 5, nr 12, s. 958-965Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The treatment of bacterial infections is increasingly complicated because microorganisms can develop resistance to antimicrobial agents. This article discusses the information that is required to predict when antibiotic resistance is likely to emerge in a bacterial population. Indeed, the development of the conceptual and methodological tools required for this type of prediction represents an important goal for microbiological research. To this end, we propose the establishment of methodological guidelines that will allow researchers to predict the emergence of resistance to a new antibiotic before its clinical introduction.

  • 12. Philippot, Laurent
    et al.
    Andersson, Siv G. E.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för evolution, genomik och systematik, Molekylär evolution.
    Battin, Tom J.
    Prosser, James I.
    Schimel, Joshua P.
    Whitman, William B.
    Hallin, Sara
    The ecological coherence of high bacterial taxonomic ranks2010Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 8, nr 7, s. 523-529Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The species is a fundamental unit of biological organization, but its relevance for Bacteria and Archaea is still hotly debated. Even more controversial is whether the deeper branches of the ribosomal RNA-derived phylogenetic tree, such as the phyla, have ecological importance. Here, we discuss the ecological coherence of high bacterial taxa in the light of genome analyses and present examples of niche differentiation between deeply diverging groups in terrestrial and aquatic systems. The ecological relevance of high bacterial taxa has implications for bacterial taxonomy, evolution and ecology.

  • 13.
    Sandegren, Linus
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Andersson, Dan I.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Bacterial gene amplification: implications for the evolution of antibiotic resistance2009Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 7, nr 8, s. 578-588Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Recent data suggest that, in response to the presence of antibiotics, gene duplication and amplification (GDA) constitutes an important adaptive mechanism in bacteria. For example, resistance to sulphonamide, trimethoprim and beta-lactams can be conferred by increased gene dosage through GDA of antibiotic hydrolytic enzymes, target enzymes or efflux pumps. Furthermore, most types of antibiotic resistance mechanism are deleterious in the absence of antibiotics, and these fitness costs can be ameliorated by increased gene dosage of limiting functions. In this Review, we highlight the dynamic properties of gene amplifications and describe how they can facilitate adaptive evolution in response to toxic drugs.

  • 14.
    Sommer, Morten O. A.
    et al.
    Antibio Tx AS, DK-2800 Lyngby, Denmark.;Tech Univ Denmark, Novo Nordisk Fdn, Ctr Biosustainabil, DK-2800 Lyngby, Denmark..
    Munck, Christian
    Tech Univ Denmark, Novo Nordisk Fdn, Ctr Biosustainabil, DK-2800 Lyngby, Denmark..
    Toft-Kehler, Rasmus Vendler
    Antibio Tx AS, DK-2800 Lyngby, Denmark..
    Andersson, Dan I
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Prediction of antibiotic resistance: time for a new preclinical paradigm?2017Ingår i: Nature Reviews Microbiology, ISSN 1740-1526, E-ISSN 1740-1534, Vol. 15, nr 11, s. 688-695Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Predicting the future is difficult, especially for evolutionary processes that are influenced by numerous unknown factors. Still, this is what is required of drug developers when they assess the risk of resistance arising against a new antibiotic candidate during preclinical development. In this Opinion article, we argue that the traditional procedures that are used for the prediction of antibiotic resistance today could be markedly improved by including a broader analysis of bacterial fitness, infection dynamics, horizontal gene transfer and other factors. This will lead to more informed preclinical decisions for continuing or discontinuing the development of drug candidates.

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