## 4 Discussion
In addition, [PERSON] and colleagues conducted an expansive examination of nutrient availability and antibiotic tolerance that included OFL and C-, N-, and P-starved cultures [12]. Using 0.75 ug/mL of OFL on cultures that had been starved for 2 h, C starvation produced the highest enhancement in tolerance, although all three starvation conditions exhibited increased survival compared to a complete media control [12]. Importantly, RecA was found to be critical to OFL tolerance of cultures in growth-supporting media, after an overnight incubation, as well as those that were resuspended in MOPS base, which reflected a role for HR that was independent of the pre-growth and treatment environments [12]. In this study, we aimed to investigate longer periods of starvation (16 h) and compare a variety of types of nutrient limitation for their persistence phenotype and dependence on DNA repair (Tables 1 and 2). Results indicated that regardless of the missing nutrient (C, N, P, or Mg\({}^{2+}\)) persistence increased in comparison to growing cultures, which was expected. We also observed that persister levels in growth-inhibited populations differed based on both the type of starvation and specific FQ used, which was unexpected and suggested that the environmental context even for non-growing bacteria matters for persistence to FQs. Here, we did not investigate the mechanisms of why different starvation types and FQs yielded quantitatively different persister levels, although those differences do represent an interesting area of study. Rather, inspired by previous studies that had shown that persistence to FQs in non-growing bacteria depended on the SOS response and DNA repair enzymes, we assayed several mutants defective in DNA repair and SOS induction [23; 24; 34; 35; 37; 65]. Those genes included _recA_, which is a master mediator of HR and SOS induction [41; 66]; _lexA_, which regulates the SOS response [43]; _recB_, which is involved in HR [42]; _ruvA_, which is involved in the final steps of recombination [47]; _uvrD_, which is involved in nucleotide excision repair [44; 45]; _recF_, which helps load RecA onto single-stranded DNA [37]; and _recN_, which stimulates strand invasion by RecA in the repair of DSBs [48]. Previously, the impacts of those genes on persistence in non-growing populations were largely investigated in C-starved conditions [23; 24; 34; 35; 37; 65] so we set out to assess their roles under deprivation of different nutrients: N, P, and Mg\({}^{2+}\) in addition to C. Our results show that regardless of the type of starvation or the FQ used, the relative importance of DNA repair machinery and the SOS response remained largely invariant. We also observed that even in cultures that did not die appreciably from treatment, N-deprived cultures in the case of LEVO and P-deprived cultures in the case of MOXI, DNA repair was critical for persister survival. The results presented here demonstrate that while the survival levels among different DNA repair mutants vary based on FQ and the starvation environment, the repair systems needed for FQ persistence in non-growing cultures are largely invariant. When this knowledge is combined with that from previous works where the importance of DNA repair machinery, such as _recA_, _recB_, _recG_, _lexA_, _ruvA_, _ruvB_, and _uvrD_, were established for FQ persistence in exponentially-growing cultures [37; 67; 68], it is straightforward to suggest that such systems can serve as universal targets for potentiation of FQs.