Lipopolysaccharide Architecture Dictates Susceptibility to Predation by Bdellovibrio bacteriovorus

Predatory bacteria such as Bdellovibrio bacteriovorus exert strong top-down control on Gram-negative bacterial populations, yet the prey surface determinants governing susceptibility to predation remain incompletely resolved. Lipopolysaccharide (LPS) is a dominant structural component of the Gram-negative outer membrane and has long been implicated in predator attachment and invasion, but how specific features of LPS architecture influence predation efficiency remains unclear. Here, the susceptibility of Escherichia coli K-12 mutants bearing defined truncations in LPS core biosynthesis was systematically examined using B. bacteriovorus 109J and three additional Bdellovibrio, HD100, BD-DH1, and EY2.3. Disruption of inner core biosynthesis genes (waaC, waaD, waaE, and waaF) or the waaG gene significantly delayed predation by all four predators. Reduced susceptibility scaled with the extent of truncation, with the shortest LPS structures conferring the greatest reduced susceptibility although none of the mutants were completely resistant and long-term killing was observed. In contrast, susceptibility to outer core truncations varied among predators, revealing strain-specific predation patterns. Restoration of O-antigen biosynthesis reduced prey susceptibility to some predators, consistent with the possibility that O-antigen sterically masks LPS-associated surface features involved in predation. Beyond its structural role, LPS also modulated predator activity. Whereas exogenous LPS acted as a decoy and delayed predation when added concomitantly with predators, pre-exposures accelerated prey killing, indicating extracellular LPS modulates predation activities and rates. Together, these findings demonstrate that the prey LPS architecture plays an important role in shaping Bdellovibrio predatory activities, with implications for predator-prey dynamics in Gram-negative microbial communities.