## 6 Discussion
Furthermore, the application of exogenous QS signaling molecules, such as acyl-homoserine lactones (AHLs), was explored to enhance electrochemical activities in bioelectrochemical systems, indicating QS's potential in bioengineering applications [265]. Collectively, these advancements underscore the pivotal role of QS in bacterial behavior and its promising exploitation in medical and industrial contexts. Ongoing advancements highlight the crucial role of sRNAs in bacterial adaptation to antibiotics by regulating resistance and tolerance mechanisms. Exposure to sub-MICs of antibiotics induces broad transcriptional and proteomic changes, including alterations in sRNA expression profiles [266]. This adaptive response enables bacteria to evade growth inhibition and develop antibiotic tolerance. Specific sRNAs have been implicated in antibiotic resistance across multiple species. In _Salmonella_ Typhimurium, for example, Giegcycline treatment induces the sRNA SroA [267], whose deletion increases susceptibility to the drug, while ectopic expression restores resistance. Similarly, in _Clostridia_, exposure to clindamycin induces an sRNA located upstream of an ABC transporter gene, conferring resistance in _Staphylococcus_ species [268]. Transcriptomic analyses of antibiotic-resistant pathogens, including Mtb, MRSA, and _P. putida_, have demonstrated that different antibiotics elicit unique sRNA expression profiles [269; 270; 271]. Some antibiotics induce extensive sRNA regulatory changes, while others influence only a limited subset of sRNAs. In _E. coli_, antibiotic stress triggers the activation of the alternative sigma factor RpoS through Hfq-dependent sRNAs such as RprA, which governs a range of stress response genes [272]. RpoS activation facilitates mutagenesis by upregulating error-prone DNA polymerase IV [273] and downregulating the DNA repair protein MutS via the sRNA SdsR. These processes enhance genetic diversity, accelerating the evolution of antibiotic resistance. Furthermore, RpoS and its associated sRNAs contribute to horizontal gene transfer by promoting plasmid conjugation, a key mechanism in the dissemination of resistance genes among bacterial populations [274]. The interplay among antibiotic exposure, sRNA regulation, and genetic adaptation underscores the critical role of sRNAs in bacterial survival and evolutionary dynamics in response to antimicrobial pressure. Expanding our understanding of sRNA dynamics reveals new strategies to combat antimicrobial resistance by targeting resistance-conferring sRNAs or disrupting key regulatory networks [275]. Synthetic antisense RNAs, for instance, could be designed to selectively inhibit sRNAs that enhance bacterial survival under antibiotic stress. Similarly, antisense oligonucleotides (ASOs) can be designed to hybridize with sRNAs, preventing their interaction with target mRNAs and thereby inhibiting their regulatory effects. CRISPR-based interventions, particularly CRISPR interference (CRISPRRi), offer another promising approach by selectively repressing sRNA expression through catalytically inactive Cas proteins [263]. Additionally, small molecules that disrupt sRNA-mRNA interactions could serve as novel antibiotics, interfering with bacterial adaptation mechanisms. These approaches highlight the growing recognition of sRNAs as viable drug targets, although challenges remain in optimizing their delivery and specificity for clinical applications. Advances in computational tools such as _sRNAdeep_[276] and _TargetRNA3_[277] have also facilitated the accurate prediction and characterization of sRNAs, enabling more precise functional studies. These machine learning-based approaches have significantly improvedthe identification of bacterial sRNAs and their regulatory targets, providing researchers with powerful tools for elucidating RNA-based regulatory mechanisms.