High lambda prophage induction in the mouse gastrointestinal tract is costly for its bacterial host
Prophages are present in the majority of bacterial strains. Although these prophages are generally considered to increase their hosts’ fitness by bringing beneficial genes, studies demonstrating such effects in ecologically relevant environments are relatively limited to few pathogenic bacterial species.
We investigated the impact of prophage carriage in the gastrointestinal tract of monoxenic mice. Combined with mathematical modelling, these experimental results provided a quantitative estimation of key parameters governing phage-bacteria interactions within this model ecosystem. We used wild-type and mutant strains of the best known host/phage pair, Escherichia coli and phage λ. Unexpectedly, λ prophage caused a significant fitness cost for its carrier, due to an induction rate 50-fold higher than in vitro, with 1 to 2 % of the prophage being induced. This high prophage induction rate reveals DNA damage-mediated SOS response in monoxenic mouse intestine.
Despite this important induction, when prophage carriers were in competition with isogenic phage susceptible bacteria, the prophage indirectly benefited its carrier by killing competitors: infection of susceptible bacteria led to phage lytic development in about 80% of cases. This effect was nevertheless very transient, since remaining infected bacteria were lysogenized, resulting overall in the rapid lysogenization of the susceptible lineage.
Due to the highly specific phage-bacteria interactions, we hypothesize that the absence of bacteria susceptible to a particular phage in the gastrointestinal tract might regularly occur, and that on the long term, the parasitic aspect of prophages prevails.
We investigated the impact of prophage carriage in the gastrointestinal tract of monoxenic mice. Combined with mathematical modelling, these experimental results provided a quantitative estimation of key parameters governing phage-bacteria interactions within this model ecosystem. We used wild-type and mutant strains of the best known host/phage pair, Escherichia coli and phage λ. Unexpectedly, λ prophage caused a significant fitness cost for its carrier, due to an induction rate 50-fold higher than in vitro, with 1 to 2 % of the prophage being induced. This high prophage induction rate reveals DNA damage-mediated SOS response in monoxenic mouse intestine.
Despite this important induction, when prophage carriers were in competition with isogenic phage susceptible bacteria, the prophage indirectly benefited its carrier by killing competitors: infection of susceptible bacteria led to phage lytic development in about 80% of cases. This effect was nevertheless very transient, since remaining infected bacteria were lysogenized, resulting overall in the rapid lysogenization of the susceptible lineage.
Due to the highly specific phage-bacteria interactions, we hypothesize that the absence of bacteria susceptible to a particular phage in the gastrointestinal tract might regularly occur, and that on the long term, the parasitic aspect of prophages prevails.
Reference:
Poster Day 3-T08-Pos-65
Session:
Posters: Virus host cell interactions, Structure/Function, Viral control of the host
Presenters:
Marianne De Paepe
Session:
Day 3 Posters Covering: Virus host cell interactions, Structure/Function, Viral control of the host
Presentation type:
Poster presentation
Room:
Poster Halls
Date:
Wednesday, 20 July 2016
Time:
12:05 - 15:30