FIGURE 1.

Formation of bacterial persistence via cell dormancy. Various pathways could trigger bacterial cells into dormant state upon antibiotic stress. A considerable number of TA modules could free toxins upon stresses, which result in persister formation by inhibiting DNA replication, or transcription, or translation processes, or downregulating proton motive force (PMF) that is under the control of SOS response. Dormancy could be also triggered by accumulated alarmone molecules and decreased intracellular ATP levels. The gray layers represent the outer membrane and inner membrane, respectively, and the red square linkage represents the peptidoglycan and periplasmic space.