Browsing by Subject "SERRATIA-MARCESCENS"

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  • Zhang, Ji; Ketola, Tarmo; Örmälä, Anni-Maria; Mappes, Johanna; Laakso, Jouni (2014)
  • Cheng, Jing; Kalliomaki, Marko; Heilig, Hans G. H. J.; Palva, Airi; Lahteenoja, Hannu; de Vos, Willem M.; Salojarvi, Jarkko; Satokari, Reetta (2013)
  • Salava, Alexander; Deptula, Paulina; Lyyski, Annina; Laine, Pia; Paulin, Lars; Väkevä, Liisa; Ranki, Annamari; Auvinen, Petri; Lauerma, Antti (2020)
  • Bruneaux, Matthieu; Ashrafi, Roghaieh; Kronholm, Ilkka; Laanto, Elina; Örmälä-Odegrip, Anni-Maria; Galarza, Juan A.; Chen, Zihan; Kubendran Sumathi, Mruthyunjay; Ketola, Tarmo (2022)
    Viruses are key actors of ecosystems and have major impacts on global biogeochemical cycles. Prophages deserve particular attention as they are ubiquitous in bacterial genomes and can enter a lytic cycle when triggered by environmental conditions. We explored how temperature affects the interactions between prophages and other biological levels using an opportunistic pathogen, the bacterium Serratia marcescens, which harbours several prophages and that had undergone an evolution experiment under several temperature regimes. We found that the release of one of the prophages was temperature-sensitive and malleable to evolutionary changes. We further discovered that the virulence of the bacterium in an insect model also evolved and was positively correlated with phage release rates. We determined through analysis of genetic and epigenetic data that changes in the bacterial outer cell wall structure possibly explain this phenomenon. We hypothezise that the temperature-dependent phage release rate acted as a selection pressure on S. marcescens and that it resulted in modified bacterial virulence in the insect host. Our study system illustrates how viruses can mediate the influence of abiotic environmental changes to other biological levels and thus be involved in ecosystem feedback loops.
  • Mikonranta, Lauri; Mappes, Johanna; Laakso, Jouni; Ketola, Tarmo (2015)
    Background: Pathogens evolve in a close antagonistic relationship with their hosts. The conventional theory proposes that evolution of virulence is highly dependent on the efficiency of direct host-to-host transmission. Many opportunistic pathogens, however, are not strictly dependent on the hosts due to their ability to reproduce in the free-living environment. Therefore it is likely that conflicting selection pressures for growth and survival outside versus within the host, rather than transmission potential, shape the evolution of virulence in opportunists. We tested the role of within-host selection in evolution of virulence by letting a pathogen Serratia marcescens db11 sequentially infect Drosophila melanogaster hosts and then compared the virulence to strains that evolved only in the outside-host environment. Results: We found that the pathogen adapted to both Drosophila melanogaster host and novel outside-host environment, leading to rapid evolutionary changes in the bacterial life-history traits including motility, in vitro growth rate, biomass yield, and secretion of extracellular proteases. Most significantly, selection within the host led to decreased virulence without decreased bacterial load while the selection lines in the outside-host environment maintained the same level of virulence with ancestral bacteria. Conclusions: This experimental evidence supports the idea that increased virulence is not an inevitable consequence of within-host adaptation even when the epidemiological restrictions are removed. Evolution of attenuated virulence could occur because of immune evasion within the host. Alternatively, rapid fluctuation between outside-host and within-host environments, which is typical for the life cycle of opportunistic bacterial pathogens, could lead to trade-offs that lower pathogen virulence.