The Central Role of Interbacterial Antagonism in Bacterial Life

Abstract

The study of bacteria interacting with their environment has historically centered on strategies for obtaining nutrients and resisting abiotic stresses. We argue this focus has deemphasized a third facet of bacterial life that is equally central to their existence: namely, the threat to survival posed by antagonizing bacteria. The diversity and ubiquity of interbacterial antagonism pathways is becoming increasingly apparent, and the insidious manner by which interbacterial toxins disarm their targets emphasizes the highly evolved nature of these processes. Studies examining the role of antagonism in natural communities reveal it can serve many functions, from facilitating colonization of naïve habitats to maintaining bacterial community stability. The pervasiveness of antagonistic pathways is necessarily matched by an equally extensive array of defense strategies. These overlap with well characterized, central stress response pathways, highlighting the contribution of bacterial interactions to shaping cell physiology. In this review, we build the case for the ubiquity and importance of interbacterial antagonism.

Figure 1.. Bacterial genomes are replete with loci encoding diverse interbacterial antagonistic pathways.

Depiction of the chromosomes of P. aeruginosa (A) and B. subtilis (B) with the position of loci encoding antagonistic factors highlighted. The loci are scaled to accurately reflect their relative lengths. Boxed schematics illustrate the function of genes within the respective element. A dashed cellular outline indicates toxin activity and arrows between two cells show toxin delivery; many loci encode factors that participate in both processes. Bacterial cell shading reflects intraspecies (light) or interspecies (dark) targeting. Values in parentheses indicate the number of genes followed by the cumulative length (in kilobases) of those genes. Factors are grouped by specific pathways (A,B) or more broadly (B), as indicated by box color and the corresponding keys.

Figure 2.. Diverse defense pathways of Gram-negative bacteria against the T6SS.

Representatives of three categories of mechanisms are highlighted. The general stress pathways Rcs and Bae respond to envelope damage brought about by cell wall targeting toxins [110], and the danger sensing Gac pathway responds to signals released from neighboring cells undergoing lysis [112]; outputs from these pathways lead to transciptional and translational changes in the cell, respectively. The defensive component(s) of the Gac regulon are not known. Within the effector-specific defenses in the rightmost portion of the cell are depicted two disparate orphan immunity mechanisms: (r)AID clusters (top) that encode effector-specific immunity proteins and ARH (ADP-ribosylhydrolase) domain proteins (bottom) that cleave the ADP-ribose moiety from targets (e.g. FtsZ) acted upon by ART (ADP-ribosyltransferase) toxins [74, 113].