## 3 Discussion  
On subsequent investigations built upon the initial findings of TA systems presence in bacteria, hundreds of genomes were examined resulting in the identification of thousands of TA systems within bacterial and archaeal genomes. These studies also unveiled  
Figure 4: (**A**) Barplot demonstrating the predicted presence and absence of the 39 gene components of TA systems detected into aEPEC, ExPEC, Hybrid, and tEPEC strains chromosomes and plasmids. Bars indicate the percentage of predicted gene presence among the bacterial strains within each pathotype. Gene predicted rate of type I, II, IV, and V TA system components present in aEPEC, ExPEC, Hybrid, and tEPEC strains in the (**B**) chromosome and in the (**C**) plasmid. Bars indicate the percentage of predicted gene presence among the bacterial strains within each TA system type. *_p_ < 0.05, as determined by a non-parametric one-way ANOVA test. new families of TA systems, and it is now acknowledged that prokaryotic genomes are thoroughly infiltrated by these genes [26]. Among the so far described eight types of TA systems, type II has been extensively researched and is prevalent in bacterial chromosomes, as well as in mobile genetic elements such as plasmids and pathogenicity islands (PAIs). Several studies have highlighted the substantial presence of these TA genes in various bacterial species. To date, experimental evidence suggests a massive presence of TA systems in pathogenic _E. coli_, but little is known regarding its distribution and function of chromosomal type II TA systems of hybrid _E. coli_ strains. In our study, the hybrid strain BA1250 exhibited a considerable number of TA systems within its bacterial genome, since we identified 26 TA loci, with 25 predicted to be located in the chromosome and only 1 in the plasmid. The identified systems were from type I, II, IV, and V, with most type II systems, reinforcing its spread among pathogenic bacteria. Similarly, one study of adherent-invasive _E. coli_ (AIEC) NRG857c strain revealed that it encodes at least 33 putative TA systems belonging to types I, II, IV, and V, distributed around all the chromosome, and some close to genomic islands [27]. The abundance of TA genes in the chromosome of pathogenic strains prompts questions about their role, specifically whether these systems play a part in bacterial virulence that provides an advantage during the infectious process. Following the identification of bacterial chromosomes, type II TA systems were initially regarded as advantageous components for adaptation, enhancing the fitness of bacterial populations during stress conditions. This occurs when the toxin is released from the toxin-antitoxin complexes due to antitoxin degradation, allowing the toxin to exert its toxic activity. This activation can result in varied outcomes depending on the model, such as stress responses or antibiotic persistence [28]. These major models were based on studies performed with _E. coli_ K-12 laboratory strains, which contain 12 type II systems. However, there is a lack of information regarding the influence of diverse stress environments on the growth dynamics of hybrid _E. coli_ strains, as well as how it alters the activation of chromosomal type II TA systems under the same conditions. The stress conditions frequently associated with TA systems are nutritional scarcity, oxidative and osmotic stress, and acid environments, all of which a hybrid _E. coli_ encounters within its host [19; 20; 21]. Consequently, hybrid strains must adapt to adverse conditions and employ different survival mechanisms. One of the earliest reports linking TA systems to stress responses was provided by [PERSON] et al. [29], demonstrating that the MazzF system was associated with the response to nutritional stress. Another study with _E. coli_ K-12, conducted by [PERSON] and colleagues [30], revealed that the expression of three TA loci was activated during severe nutritional scarcity, and two systems were activated under mild nutritional scarcity.