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  • 1.
    Barandun, Jonas
    et al.
    Laboratory of Protein and Nucleic Acid Chemistry, The Rockefeller University, New York, NY, USA; Present address: Department of Molecular Biology, The Laboratory for Molecular Infection Medicine Sweden, Umeå Centre for Microbial Research, Science for Life Laboratory, Umeå University, Umeå, Sweden.
    Hunziker, Mirjam
    Vossbrinck, Charles R.
    Klinge, Sebastian
    Evolutionary compaction and adaptation visualized by the structure of the dormant microsporidian ribosome2019In: Nature Microbiology, E-ISSN 2058-5276, Vol. 4, no 11, p. 1798-1804Article in journal (Refereed)
    Abstract [en]

    Microsporidia are eukaryotic parasites that infect essentially all animal species, including many of agricultural importance(1-3), and are significant opportunistic parasites of humane. They are characterized by having a specialized infection apparatus, an obligate intracellular lifestyles(5), rudimentary mitochondria and the smallest known eukaryotic genomess(5-7). Extreme genome compaction led to minimal gene sizes affecting even conserved ancient complexes such as the ribosomes(8-10). In the present study, the cryo-electron microscopy structure of the ribosome from the microsporidium Vairimorpha necatrix is presented, which illustrates how genome compaction has resulted in the smallest known eukaryotic cytoplasmic ribosome. Selection pressure led to the loss of two ribosomal proteins and removal of essentially all eukaryote-specific ribosomal RNA (rRNA) expansion segments, reducing the rRNA to a functionally conserved core. The structure highlights how one microsporidia-specific and several repurposed existing ribosomal proteins compensate for the extensive rRNA reduction. The microsporidian ribosome is kept in an inactive state by two previously uncharacterized dormancy factors that specifically target the functionally important E-site, P-site and polypeptide exit tunnel. The present study illustrates the distinct effects of evolutionary pressure on RNA and proteincoding genes, provides a mechanism for ribosome inhibition and can serve as a structural basis for the development of inhibitors against microsporidian parasites.

  • 2. Brugat, Thibaut
    et al.
    Reid, Adam James
    Lin, Jingwen
    Cunningham, Deirdre
    Tumwine, Irene
    Kushinga, Garikai
    McLaughlin, Sarah
    Spence, Philip
    Böhme, Ulrike
    Sanders, Mandy
    Conteh, Solomon
    Bushell, Ellen
    Metcalf, Tom
    Billker, Oliver
    Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.
    Duffy, Patrick E.
    Newbold, Chris
    Berriman, Matthew
    Langhorne, Jean
    Antibody-independent mechanisms regulate the establishment of chronic Plasmodium infection2017In: Nature Microbiology, E-ISSN 2058-5276, Vol. 2, no 4, article id UNSP 16276Article in journal (Refereed)
    Abstract [en]

    Malaria is caused by parasites of the genus Plasmodium. All human-infecting Plasmodium species can establish long-lasting chronic infections(1-5), creating an infectious reservoir to sustain transmission(1,6). It is widely accepted that the maintenance of chronic infection involves evasion of adaptive immunity by antigenic variation(7). However, genes involved in this process have been identified in only two of five human-infecting species: Plasmodium falciparum and Plasmodium knowlesi. Furthermore, little is understood about the early events in the establishment of chronic infection in these species. Using a rodent model we demonstrate that from the infecting population, only a minority of parasites, expressing one of several clusters of virulence-associated pir genes, establishes a chronic infection. This process occurs in different species of parasites and in different hosts. Establishment of chronicity is independent of adaptive immunity and therefore different from the mechanism proposed for maintenance of chronic P. falciparum infections(7-9). Furthermore, we show that the proportions of parasites expressing different types of pir genes regulate the time taken to establish a chronic infection. Because pir genes are common to most, if not all, species of Plasmodium(10), this process may be a common way of regulating the establishment of chronic infections.

  • 3.
    Brussaard, Corina P. D.
    et al.
    NIOZ Royal Netherlands Institute of Sea Research, Netherlands ; University of Utrecht, Netherlands.
    Bidle, Kay D.
    Rutgers University, USA.
    Pedrós-Alió, Carlos
    Institut de Ciències del Mar (CSIC), Spain.
    Legrand, Catherine
    Linnéuniversitetet, Institutionen för biologi och miljö (BOM).
    The interactive microbial ocean2016In: Nature Microbiology, E-ISSN 2058-5276, Vol. 2, article id 16255Article in journal (Refereed)
    Abstract [en]

    Marine microorganisms inhabit diverse environments and interact over different spatial and temporal scales. To fully understand how these interactions shape genome structures, cellular responses, lifestyles, community ecology and biogeochemical cycles, integration of diverse approaches and data is essential.

  • 4.
    Bueno, Emilio
    et al.
    Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS).
    Sit, Brandon
    Waldor, Matthew K.
    Cava, Felipe
    Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS). Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
    Anaerobic nitrate reduction divergently governs population expansion of the enteropathogen Vibrio cholerae2018In: Nature Microbiology, E-ISSN 2058-5276, Vol. 3, no 12, p. 1346-1353Article in journal (Refereed)
    Abstract [en]

    To survive and proliferate in the absence of oxygen, many enteric pathogens can undergo anaerobic respiration within the host by using nitrate (NO3-) as an electron acceptor(1,2). In these bacteria, NO3- is typically reduced by a nitrate reductase to nitrite (NO2-), a toxic intermediate that is further reduced by a nitrite reductase(3). However, Vibrio cholerae, the intestinal pathogen that causes cholera, lacks a nitrite reductase, leading to NO2- accumulation during nitrate reduction 4(.) Thus, V. cholerae is thought to be unable to undergo NO3-(-)dependent anaerobic respiration(4). Here, we show that during hypoxic growth, NO3- reduction in V. cholerae divergently affects bacterial fitness in a manner dependent on environmental pH. Remarkably, in alkaline conditions, V. cholerae can reduce NO3- to support population growth. Conversely, in acidic conditions, accumulation of NO2- from NO3- reduction simultaneously limits population expansion and preserves cell viability by lowering fermentative acid production. Interestingly, other bacterial species such as Salmonella typhimurium, enterohaemorrhagic Escherichia coli (EHEC) and Citrobacter rodentium also reproduced this pH-dependent response, suggesting that this mechanism might be conserved within enteric pathogens. Our findings explain how a bacterial pathogen can use a single redox reaction to divergently regulate population expansion depending on the fluctuating environmental pH.

  • 5. Javaheri, Anahita
    et al.
    Kruse, Tobias
    Moonens, Kristof
    Mejias-Luque, Raquel
    Debraekeleer, Ayla
    Asche, Carmen I.
    Tegtmeyer, Nicole
    Kalali, Behnam
    Bach, Nina C.
    Sieber, Stephan A.
    Hill, Darryl J.
    Koeniger, Verena
    Hauck, Christof R.
    Moskalenko, Roman
    Haas, Rainer
    Busch, Dirk H.
    Klaile, Esther
    Slevogt, Hortense
    Schmidt, Alexej
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Medical Faculty, Institute of Anatomy, University Duisburg-Essen, 45122 Essen, Germany.
    Backert, Steffen
    Remaut, Han
    Singer, Bernhard B.
    Gerhard, Markus
    Helicobacter pylori adhesin HopQ engages in a virulence-enhancing interaction with human CEACAMs2017In: Nature Microbiology, E-ISSN 2058-5276, Vol. 2, no 1, article id 16189Article in journal (Refereed)
    Abstract [en]

    Helicobacter pylori specifically colonizes the human gastric epithelium and is the major causative agent for ulcer disease and gastric cancer development. Here, we identify members of the carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family as receptors of H. pylori and show that HopQ is the surface-exposed adhesin that specifically binds human CEACAM1, CEACAM3, CEACAM5 and CEACAM6. HopQ-CEACAM binding is glycan-independent and targeted to the N-domain. H. pylori binding induces CEACAM1-mediated signalling, and the HopQ-CEACAM1 interaction enables translocation of the virulence factor CagA into host cells and enhances the release of pro-inflammatory mediators such as interleukin-8. Based on the crystal structure of HopQ, we found that a beta-hairpin insertion (HopQ-ID) in HopQ's extracellular 3+4 helix bundle domain is important for CEACAM binding. A peptide derived from this domain competitively inhibits HopQ-mediated activation of the Cag virulence pathway, as genetic or antibody-mediated abrogation of the HopQ function shows. Together, our data suggest the HopQ-CEACAM1 interaction to be a potentially promising novel therapeutic target to combat H. pylori-associated diseases.

  • 6. Kent, Robyn S
    et al.
    Modrzynska, Katarzyna K
    Cameron, Rachael
    Philip, Nisha
    Billker, Oliver
    Wellcome Trust Sanger Institute, Hinxton, Cambridge, UK.
    Waters, Andrew P
    Inducible developmental reprogramming redefines commitment to sexual development in the malaria parasite Plasmodium berghei2018In: Nature Microbiology, E-ISSN 2058-5276, Vol. 3, no 11, p. 1206-1213Article in journal (Refereed)
    Abstract [en]

    During malaria infection, Plasmodium spp. parasites cyclically invade red blood cells and can follow two different developmental pathways. They can either replicate asexually to sustain the infection, or differentiate into gametocytes, the sexual stage that can be taken up by mosquitoes, ultimately leading to disease transmission. Despite its importance for malaria control, the process of gametocytogenesis remains poorly understood, partially due to the difficulty of generating high numbers of sexually committed parasites in laboratory conditions1. Recently, an apicomplexa-specific transcription factor (AP2-G) was identified as necessary for gametocyte production in multiple Plasmodium species2,3, and suggested to be an epigenetically regulated master switch that initiates gametocytogenesis4,5. Here we show that in a rodent malaria parasite, Plasmodium berghei, conditional overexpression of AP2-G can be used to synchronously convert the great majority of the population into fertile gametocytes. This discovery allowed us to redefine the time frame of sexual commitment, identify a number of putative AP2-G targets and chart the sequence of transcriptional changes through gametocyte development, including the observation that gender-specific transcription occurred within 6 h of induction. These data provide entry points for further detailed characterization of the key process required for malaria transmission.

  • 7. Omattage, Natalie S.
    et al.
    Deng, Zengqin
    Pinkner, Jerome S.
    Dodson, Karen W.
    Almqvist, Fredrik
    Umeå University, Faculty of Science and Technology, Department of Chemistry. Umeå University, Faculty of Medicine, Umeå Centre for Microbial Research (UCMR).
    Yuan, Peng
    Hultgren, Scott J.
    Structural basis for usher activation and intramolecular subunit transfer in P pilus biogenesis in Escherichia coli2018In: Nature Microbiology, E-ISSN 2058-5276, Vol. 3, no 12, p. 1362-1368Article in journal (Refereed)
    Abstract [en]

    Chaperone-usher pathway pili are extracellular proteinaceous fibres ubiquitously found on Gram-negative bacteria, and mediate host-pathogen interactions and biofilm formation critical in pathogenesis in numerous human diseases(1). During pilus assembly, an outer membrane macromolecular machine called the usher catalyses pilus biogenesis from the individual subunits that are delivered as chaperone-subunit complexes in the periplasm. The usher orchestrates pilus assembly using all five functional domains: a 24-stranded transmembrane beta-barrel translocation domain, a beta-sandwich plug domain, an amino-terminal periplasmic domain and two carboxy-terminal periplasmic domains (CTD1 and CTD2)(2-6). Despite extensive structural and functional characterization, the mechanism by which the usher is activated to initiate pilus biogenesis is unknown. Here, we present the crystal structure of the full-length PapC usher from Escherichia coli in complex with its cognate PapDG chaperone-subunit complex in a pre-activation state, elucidating molecular details of how the usher is specifically engaged by allosteric interactions with its substrate preceding activation and how the usher facilitates the transfer of subunits from the amino-terminal periplasmic domain to the CTDs during pilus assembly. This work elucidates the intricate workings of a molecular machine that catalyses chaperone-usher pathway pilus assembly and opens the door for the development of potent inhibitors to block pilus biogenesis.

  • 8. Ramirez, Kelly S.
    et al.
    Knight, Christopher G.
    de Hollander, Mattias
    Brearley, Francis Q.
    Constantinides, Bede
    Cotton, Anne
    Creer, Si
    Crowther, Thomas W.
    Davison, John
    Delgado-Baquerizo, Manuel
    Dorrepaal, Ellen
    Umeå University, Faculty of Science and Technology, Department of Ecology and Environmental Sciences.
    Elliott, David R.
    Fox, Graeme
    Griffiths, Robert I.
    Hale, Chris
    Hartman, Kyle
    Houlden, Ashley
    Jones, David L.
    Krab, Eveline J.
    Umeå University, Faculty of Science and Technology, Department of Ecology and Environmental Sciences.
    Maestre, Fernando T.
    McGuire, Krista L.
    Monteux, Sylvain
    Umeå University, Faculty of Science and Technology, Department of Ecology and Environmental Sciences.
    Orr, Caroline H.
    van der Putten, Wim H.
    Roberts, Ian S.
    Robinson, David A.
    Rocca, Jennifer D.
    Rowntree, Jennifer
    Schlaeppi, Klaus
    Shepherd, Matthew
    Singh, Brajesh K.
    Straathof, Angela L.
    Bhatnagar, Jennifer M.
    Thion, Cecile
    van der Heijden, Marcel G. A.
    de Vries, Franciska T.
    Detecting macroecological patterns in bacterial communities across independent studies of global soils2018In: Nature Microbiology, E-ISSN 2058-5276, Vol. 3, no 2, p. 189-196Article in journal (Refereed)
    Abstract [en]

    The emergence of high-throughput DNA sequencing methods provides unprecedented opportunities to further unravel bacterial biodiversity and its worldwide role from human health to ecosystem functioning. However, despite the abundance of sequencing studies, combining data from multiple individual studies to address macroecological questions of bacterial diversity remains methodically challenging and plagued with biases. Here, using a machine-learning approach that accounts for differences among studies and complex interactions among taxa, we merge 30 independent bacterial data sets comprising 1,998 soil samples from 21 countries. Whereas previous meta-analysis efforts have focused on bacterial diversity measures or abundances of major taxa, we show that disparate amplicon sequence data can be combined at the taxonomy-based level to assess bacterial community structure. We find that rarer taxa are more important for structuring soil communities than abundant taxa, and that these rarer taxa are better predictors of community structure than environmental factors, which are often confounded across studies. We conclude that combining data from independent studies can be used to explore bacterial community dynamics, identify potential 'indicator' taxa with an important role in structuring communities, and propose hypotheses on the factors that shape bacterial biogeography that have been overlooked in the past.

  • 9. Zehr, Jonathan P.
    et al.
    Shilova, Irina N.
    Farnelid, Hanna M.
    Munoz-Marin, Maria del Carmen
    Turk-Kubo, Kendra A.
    Unusual marine unicellular symbiosis with the nitrogen-fixing cyanobacterium UCYN-A (vol 2, 16214, 2016)2017In: Nature Microbiology, E-ISSN 2058-5276, Vol. 2, no 3, article id 17016Article in journal (Refereed)
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