## 1 Introduction  
Bacterial persistence is increasingly recognized as one of the major causes of antibiotic treatment failure and recurrence of infections [1, 2]. Persisters are a subpopulation of slow-growing or growth-arrested bacterial cells with a decreased susceptibility to bactericidal antibiotics within a susceptible clonal population [3]. Antibiotic persistence is an ability widely described in bacterial species irrespective of whether they possess genes enabling antibiotic resistance [3, 4, 5]. However, the underlying mechanism of persister production is a complex and still unclear phenomenon that includes multiple systems and pathways such as the (p)ppGpp-mediated stringent response, toxin-antitoxins (TA), SOS response to DNAdamage, RpoS-mediated general stress response, modulation of energy metabolism, and drug efflux pumps [1; 6; 7]. In recent years, some studies have explored the participation of the small RNA (sRNA) chaperone Hfq in antibiotic persistence, showing differences among bacteria and conditions [5; 7; 8]. Hfq is conserved in a wide range of bacteria and regulates several physiological processes to maintain intracellular homeostasis [9]. The importance of Hfq under stressful environments is evident from the pleiotropic effects observed when the _Hfq_ gene is inactivated in different bacteria. The _hfq_ gene disruption produces a decreased growth rate, cell filamentation, and increased sensitivity to stresses and alters motility and biofilm formation [9]. The regulatory role of Hfq on antibiotic persistence is still a poorly explored field and differs from one species to another [5; 7; 8]. For instance, _Escherichia coli_\(\Delta\)_lfq_ persister cells formation capacity increases when challenged by ampicillin [8], and defective persistence increases following exposure to gentamicin, levofloxacin or cefotaxime [7]. In the case of the fish pathogen _Aeromonas veronii_, _hfq_ deletion plays a negative role in persister cells formation under the treatments of tetracycline, cefotaxime, ciprofloxacin and chloramphenicol [5].  
_Yersinia ruckeri_ is a facultative, Gram-negative pathogen responsible for the enteric redmouth disease (ERM), a severe septicemic disease that mainly affects salmonids and, consequently, the fish farming industry. In recent years, the number of outbreaks provoked by this pathogen has substantially increased in the aquaculture sector [10], affecting fish in all development stages and exhibiting higher mortality in adult specimens [11]. The ability of _Y. ruckeri_ to survive in fish farms is based on its adaptation to disadvantage environmental conditions such as antibiotic exposure [12]. The most commonly used antibiotics worldwide, such as prophylaxis and to treat ERM outbreaks, include oxyetracycline, florfenicol, oxolinite acid, amoxicillin and sulfadiazine, in combination with trimethoprim [13; 14; 15; 16]. In vitro studies have demonstrated that _Y. ruckeri_ can develop resistance to oxolinite acid, oxytetracycline and the potentiated sulphonamide [17]. However, to our knowledge, studies focused on antibiotic persistence in this pathogen have not been reported to date. To investigate the regulatory role of _Y. ruckeri_ Hfq in antibiotic persistence, we compared _Y. ruckeri_ wild-type and \(\Delta\)_lfq_ regarding their growth and metabolic status, the susceptibility to sublethal concentrations of bactericidal antibiotics, and persister cells production upon exposure to lethal concentrations of such antibiotics. Furthermore, to better understand the participation of Hfq in antibiotic persistence, its dependence on _relA_ ((p)ppGpp synthetase encoding gene) was also analyzed. Our results provide evidence for the participation of Hfq from _Y. ruckeri_ in antibiotic persistence and contribute to understanding the phenomenon of antibiotic persistence in this salmonid pathogen.