Abortive infection antiphage defense systems: separating mechanism and phenotype.

Abstract

Bacteria have evolved a wide array of mechanisms that allow them to eliminate phage infection. 'Abortive infection' (abi) systems are an expanding category of such mechanisms, defined as those which induce programmed cell death (or dormancy) upon infection, and thus halt phage propagation within a bacterial population. This definition entails two requirements - a phenotypic observation (cell death upon infection), and a mechanistic determination of its sources (system-induced death). The phenotypic and mechanistic aspects of abi are often implicitly assumed to be tightly linked, and studies regularly tend to establish one and deduce the other. However, recent evidence points to a complicated relationship between the mechanism of defense and the phenotype observed upon infection. We argue that rather than viewing the abi phenotype as an inherent quality of a set of defense systems, it should be more appropriately thought of as an attribute of interactions between specific phages and bacteria under given conditions. Consequently, we also point to potential pitfalls in the prevailing methods for ascertaining the abi phenotype. Overall, we propose an alternative framework for parsing interactions between attacking phages and defending bacteria.