Bacterial addiction module toxin Doc inhibits translation elongation through its association with the 30S ribosomal subunit.

ABSTRACT: Bacterial toxin-antitoxin (TA) systems (or "addiction modules") typically facilitate cell survival during intervals of stress by inducing a state of reversible growth arrest. However, upon prolonged stress, TA toxin action leads to cell death. TA systems have also been implicated in several clinically important phenomena: biofilm formation, bacterial persistence during antibiotic treatment, and bacterial pathogenesis. TA systems harbored by pathogens also serve as attractive antibiotic targets. To date, the mechanism of action of the majority of known TA toxins has not yet been elucidated. We determined the mode of action of the Doc toxin of the Phd-Doc TA system. Doc expression resulted in rapid cell growth arrest and marked inhibition of translation without significant perturbation of tr

SUBMITTER: Liu M 

PROVIDER: S-EPMC2311363 | biostudies-literature | 2008 Apr

REPOSITORIES: biostudies-literature