## 1 Introduction  
Nutrient limitation is a stress that bacteria can experience in a host [1, 2, 3]. For example, in the urinary tract, which is a common site of infections [4], urine constitutes a poor growth medium, since it lacks glucose, contains high concentrations of urea, and low levels of peptides and amino acids [1, 5]. Throughout the body, phagocytes use nutrient deprivation as part of their antibacterial strategy for internalized pathogens [2, 6, 7]. Phagosomes have shown to be deficient in carbon, amino acids, nucleotides, and vitamins [2, 7]. Further, when bacteria reside in biofilms or multicellular aggregates, nutrient gradients can arise depending on the chemical composition of the surroundings and metabolic activities of cells, which can produce starvation in some resident bacteria [8, 9]. Importantly, the antibiotic tolerances of starved bacteria often exceed those of their growing counterparts, which contributes to the difficulties in treating nutrient-deprived bacteria effectively [10, 11, 12, 13]. Although starvation, regardless of the type, has the common end-point of growth inhibition, the physiology of bacteria in growth arrest will depend on the limiting nutrient or nutrients [14, 15, 16, 17]. For example, during glucose starvation the levels of regulatory metabolites cyclic AMP (cAMP) [18], guanosine 3\({}^{\prime}\), 5\({}^{\prime}\)-bisphrophosph (ppGpp) [19], and phosphoenolpyruvate (PEP) increase, whereas fructose 1,6-biphosphate (FBP) levels decrease [15, 16]; and each regulates a different suite of activities [14]. During nitrogen (N) starvation, while an increase in ppGpp has been observed, cAMP and FBP levels appear unaffected, and PEP levels decline [15]. Heat production, CO\({}_{2}\) generation, and O\({}_{2}\) consumption differ between carbon (C)-, N-, and phosphate (P)-starved cultures [20], whereas glucose consumption varies between N-, P-, and Mg\({}^{2+}\)-starved populations, with Mg\({}^{2+}\)-starved cultures catabolizing glucose at the highest rate [16]. With such metabolic and regulatory differences,it is not surprising that the antibiotic susceptibilities of nutrient-depleted bacteria will depend on the missing nutrient. For example, with the aminoglycoside gentamicin, N- and P-starved cultures showed a notable level of susceptibility, whereas C-starved cultures were extremely tolerant [21]. In a study with nitrofurantoin, when stationary-phase bacteria were resuspended in saline, only C-supplied bacteria became sensitive to the antibiotic, whereas N-, P-, and Mg\({}^{2+}\)-supplied bacteria remained completely tolerant [22]. Collectively, these studies suggest that while growth inhibition in general increases the tolerances of bacteria to antibiotics, it may not do so in a uniform fashion. Here, we examine how fluoroquinoline (FQ) persistence varies in growth-inhibited populations based on the identity of the missing nutrient. While most antibiotics are ineffective against non-growing bacteria, FQs, which target type II topoisomerases (DNA gyrase and topoisomerase IV), retain bactericidal activity [23; 24; 25]. During its catalytic cycle, topoisomerases produce transient breaks in DNA to modulate supercoiling, and consume two equivalents of ATP along the way [26; 27; 28; 29]. Conceivably, differences in ATP could alter the activities of DNA gyrase and topoisomerase IV, which could impact sensitivity to FQs. Inspired by the physiological differences that have been observed between bacteria starved for different nutrients [14; 15; 16; 17; 18; 19], we hypothesized that persistence to FQ will depend on the missing nutrient. Persistence is an extreme form of antibiotic tolerance that is exhibited by subpopulations in a bacterial culture [30; 31; 32], and most studies that have investigated FQ persistence in growth-inhibited populations have done so with stationary-phase cultures, which typically experience growth arrest due to exhaustion of carbon [23; 24; 25; 33; 34; 35; 36; 37; 38; 39; 40].