Molecular mechanisms of multiple toxin-antitoxin systems are coordinated to govern the persister phenotype.

ABSTRACT: Toxin-antitoxin systems are ubiquitous and have been implicated in persistence, the multidrug tolerance of bacteria, biofilms, and, by extension, most chronic infections. However, their purpose, apparent redundancy, and coordination remain topics of debate. Our model relates molecular mechanisms to population dynamics for a large class of toxin-antitoxin systems and suggests answers to several of the open questions. The generic architecture of toxin-antitoxin systems provides the potential for bistability, and even when the systems do not exhibit bistability alone, they can be coupled to create a strongly bistable, hysteretic switch between normal and toxic states. Stochastic fluctuations can spontaneously switch the system to the toxic state, creating a heterogeneous population of growing

SUBMITTER: Fasani RA 

PROVIDER: S-EPMC3703989 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature