Persisters are cells which evade stresses like antibiotics and which are characterized by reduced metabolism and a lack of genetic alterations required to achieve this state We showed previously that MqsR and MqsA of Escherichia colt are a toxin-antitoxin pair that influence cell physiology (e.g, biofilm formation and motility) via RNase activity as well as through regulation of toxin CspD Here,we show that deletion of the mqsRA locus decreases persister cell formation and. consistent with this result. over production of MqsR increases persister cell formation Furthermore, toxins Hha, CspD, and HokA increase persister cell formation In addition, by overproducing MqsR in a series of isogenic Mutants. we show that Hha and CspD are necessary for persister cell Formation via MqsR overexpression. Surprisingly, Hfq, a small RNA chaperone, decreases persistence A whole-transcriptome Study shows that Hfq induces transport-related genes (opp genes and dppA). outer membrane protein-related genes (ybfM and ybfN), toxins (hha), and proteases (clpX, clpP, and Ion) Taken together, these results indicate that toxins CspD, Hha. and HokA influence persister cell formation via MqsR and that Hfq plays an important role in the regulation of persister cell formation via regulation of transport or outer membrane proteins OppA and YbfM (c) 2009 Elsevier Inc. All rights reserved