dependent on the T6SS, as deletion of vasK or vasH abrogated
bacterial killing (Fig. 2A). T6SS-mediated virulence toward
E. coli was restored in the complemented strains V52ΔvasK/
pvasK and V52ΔvasH/pvasH (Fig. 2A).
To observe the kinetics of bacterial killing and further validate
the previous results, E. coli survival was measured at multiple
time intervals during exposure to V52 at a multiplicity of infection
(MOI) of 1 and 10 (Fig. 2B). The resulting survival curves
show a progressive reduction in E. coli survival due to extended
exposure to wild-type V52 (Fig. 2B). Addition of V52 at a MOI
of 10 and 1 caused 10,000- and 1,000-fold reductions in E. coli,
respectively (Fig. 2B). Maximum killing occurred within 2 h,
followed by the persistence of a smaller number of E. coli for the
remaining exposure time (Fig. 2B).
Next we tested whether the addition of fresh V52 predator at
the 2-h time point could eliminate or reduce the number of persistent
E. coli survivors. Exposing E. coli prey to a second dose of
V52 at the 2-h time point did not drastically affect the survival of
E. coli and 102 cfu·mL−1 remained after 6 h (Fig. S2).