## 1 Introduction
sRNAs are involved in key cellular processes, including the regulation of bacteria transport through the modulation of outer membrane protein expression, iron homeostasis, quorum sensing, and bacterial virulence [23; 24; 25; 26; 27]. Advancements in bioinformatics and experimental methodologies have facilitated the discovery of over 900 bacterial sRNAs, primarily transcribed from intergenic regions [28]. These sRNAs are classified as either cis-encoded or trans-encoded based on their genomic arrangement relative to target genes. Cis-encoded sRNAs are transcribed from the same genomic locus as their target mRNA and typically exhibit perfect complementarity. In contrast, trans-encoded sRNAs are transcribed from separate loci and regulate multiple targets with partial complementarity, often requiring RNA chaperones like Hfq [29; 30]. Computational approaches, including comparative genomics and machine learning-based predictions, have significantly improved sRNA identification and target prediction, although experimental validation remains essential due to challenges posed by imperfect base pairing in trans-encoded sRNAs. The continued discovery and functional characterization of sRNAs are critical to understanding their roles in bacterial stress response and pathogenesis [31]. Bacteria encounter numerous stressors within the host environment, including nutrient deprivation, temperature fluctuations, oxidative stress, osmotic pressure changes, and exposure to antimicrobial compounds [32; 33]. To mitigate the harmful effects of the aforementioned host response, bacteria have developed intricate stress response pathways regulated through transcriptional control by sigma factors and two-component systems [34; 35; 36]. The discovery of sRNAs has unveiled an additional layer of posttranscriptional regulation, enabling bacteria to fine-tune gene expression with high precision and efficiency. These small RNAs regulate the expression of their target gene by altering mRNA stability, translation, and processing, allowing rapid adaptation to environmental changes. By coordinating cellular processes such as metabolic reprogramming [37; 38], detoxification [39], DNA repair [40], and biofilm formation [41; 42], sRNAs serve as pivotal regulators of bacterial stress responses. Beyond stress adaptation, sRNAs also play a central role in bacterial virulence, governing the expression of key pathogenicity determinants, including toxins [43], adhesins, invasins [44], and immune evasion factors [45]. Furthermore, sRNAs have been shown to play a key role in antimicrobial resistance, one of the pressing global concerns. The rise in antimicrobial resistance (AMR) where the pathogenic bacteria become resistant to multiple drugs represents a significant global health threat, with resistant infections leading to increased morbidity, mortality, and healthcare costs [46]. The World Health Organization (WHO) has identified 24 priority pathogens exhibiting significant resistance, including AMR Mtb and Gram-negative bacteria resistant to last-line antibiotics [47]. Projections indicate that AMR could result in approximately 39 million deaths between 2025 and 2050, underscoring the urgency of addressing this crisis. While mechanisms such as horizontal gene transfer and mutations in antibiotic target sites have been extensively studied [48; 49], recent research has identified sRNAs as important contributors to antimicrobial resistance [50; 51]. These sRNAs influence antibiotic resistance through multiple pathways including the modification of cell membrane components, the repression of antibiotic uptake systems, the activation of efflux pumps, and the generation of biofilms [51]. In addition, bacteria can also achieve antimicrobial resistance through an alternative mechanism--quorum sensing [52]. This process enables bacteria to respond to specific chemical messengers by fine-tuning the expression of genes involved in biofilm formation and antimicrobial resistance, allowing them to adapt to changing environmental conditions [52].