Thioredoxin 1 moonlights as a chaperone for an interbacterial ADP-ribosyltransferase toxin.

Formation and breakage of disulfide bridges strongly impacts folding and activity of proteins. Thioredoxin 1 (TrxA) is a small, conserved enzyme that reduces disulfide bonds in the bacterial cytosol. In this study, we provide an example of the emergence of a chaperone role for TrxA, which is independent of redox catalysis.

TisB protein is the single molecular determinant underlying multiple downstream effects of ofloxacin in .

Bactericidal antibiotics can cause metabolic perturbations that contribute to antibiotic-induced lethality. The molecular mechanism underlying these downstream effects remains unknown. Here, we show that ofloxacin, a fluoroquinolone that poisons DNA gyrase, induces a cascade of metabolic changes that are dependent on an active SOS response.

Single-cell evidence for plasmid addiction mediated by toxin-antitoxin systems.

Toxin-antitoxin (TA) systems are small selfish genetic modules that increase vertical stability of their replicons. They have long been thought to stabilize plasmids by killing cells that fail to inherit a plasmid copy through a phenomenon called post-segregational killing (PSK) or addiction. While this model has been widely accepted, no direct observation of PSK was reported in the literature.

Are envelope stress responses essential for persistence to β-lactams in ?

Bacterial persistence to antibiotics defines the ability of small sub-populations of sensitive cells within an isogenic population to survive high doses of bactericidal antibiotics. Here, we investigated the importance of the five main envelope stress responses (ESRs) of in persistence to five bactericidal β-lactam antibiotics by combining classical time-kill curve experiments and single-cell analysis using time-lapse microscopy. We showed that the survival frequency of mutants for the Bae, Cpx, Psp, and Rcs systems treated with different β-lactams is comparable to that of the wild-type strain, indicating that these ESRs do not play a direct role in persistence to β-lactams.

Population and Single-Cell Analysis of Antibiotic Persistence in Escherichia coli.

Antibiotic persistence refers to the capacity of small bacterial subpopulations to transiently tolerate high doses of bactericidal antibiotics. Upon bactericidal antibiotic treatment, the bulk of the bacterial population is rapidly killed. This first rapid phase of killing is followed by a substantial decrease in the rate of killing as the persister cells remain viable.