## 1 Introduction  
Actively growing populations of bacteria harbor a subpopulation of dormant cells [1, 2]. These cells are insensitive to the action of antibiotics and other stresses [3, 4]. Once stress is removed, dormant cells can resume growth, and the population will again become a mixture of actively growing and dormant cells. This phenomenon of forming a persistent subpopulation is distinctive from antibiotic resistance, which involves genetic changes. Persister cells are of clinical importance, as these cells are responsible for recurring infections [3]. Recent studies suggest that reduction of the growth rate via inhibition of a core cellular activity can create a non-growing, persistent subpopulation [5, 6]. HipA is a toxin of a TA system on the _E. coli_ genome [7]. TA systems are small genetic modules that are ubiquitously found in bacterial genomes [8, 9]. TA modules are composed of a pair of co-transcribed toxin and antitoxin genes [8]. In type II TA systems, toxin proteins target a variety of essential cellular processes, including protein translation, DNA replication and cell division [10, 11, 12, 13, 14, 15]. Antitoxins sequester toxins from their targets via the formation of a stable complex until the stress-inducible proteases, such as Lon, preferentially degrade the antitoxin proteins, freeing the toxin proteins to exert their inhibitory activity [16, 17]. A gain-of-function mutant allele of _hipA_ (_hipA_7) was first identified as a genetic locus responsible for a high proportion of persister cells [7]. HipA is a kinase [18, 19]. HipA7 is encoded from a mutant allele (_hipA7_) harboring two amino acid substitutions [20]. HipA7 encoded endogenously from the chromosome is shown to phosphorylate Glu-tRNA-ligase (GltX) [21]. Phosphorylation inhibits GltX activity, which increases the amount of uncharged tRNA(Glu) [19]. This, in turn, induces a stringent response (i.e., increase in the ppGpp levels via RelA/SpoT) [19], leading to the inhibition of transcription, translation, replication and cell wall synthesis. As a result, cells halt growth and become dormant [19]. When wildtype _hipA_ was expressed endogenously from the chromosome, the phosphorylation of GltX was not observed [21]. It is proposed that this is because HipA forms a complex with co-expressed antitoxin HipB. When wildtype _hipA_ was expressed at a higher level via ectopic expression, GltX phosphorylation was observed [19; 21]. The results demonstrate that a higher level of free HipA than HipB is necessary to inhibit its target(s). A direct tie between _hipA_ expression and growth arrest has been demonstrated. HipA overexpression halts cells growth, which can be reversed by the expression of HipB [22]. A single-cell study of _hipA_ revealed that the concentration of HipA needs to exceed a threshold to induce growth arrest [23]. Stochastic variations in the HipA level within a population creates a mixture of dormant and actively growing cells. The authors also showed that the length of dormancy depends on the level of HipA. Furthermore, the overexpression of GltX can reverse the _hipA_-induced toxicity, validating the link between _hipA_-induced cell growth arrest and inhibition of GltX [18; 19]. The overexpression of _hipA_ in cells grown in liquid medium exhibit a unique growth curve [22]. The growth arrest is transient despite the continuous presence of inducers. Following a few hours of arrest, cells resume growth even without the ectopic induction of HipB [22]. The same growth pattern has not been seen for other TA toxins, such as YoeB, YeeV and CptA [11; 24; 25]. In such cases, growth arrest continues until cells become no longer viable. While memory or learning is traditionally linked to multicellular organisms, recent studies suggest that these behaviors exist even in single-cellular organisms, such as bacteria. Bacterial regulatory networks exhibit complex dynamics and multi-stable behaviors, which are the hallmark of memory in other organisms [26; 27].