However, some genes that were downregulated in 13124R were upregulated in NCTRR. qRT-PCR analysis confirmed that the transcription of these genes, which included toxin genes for phospholipase C (PLC),
perfringolysin O (PFO), collagenase and clostripain, were affected differently in the two mutants. Similarly, the production of these enzymes and the toxicity see more of the culture supernatants decreased in 13124R and increased in NCTRR. It appears that gatifloxacin resistance selection resulted in alteration of global gene transcription in C. perfringens and that the effect was strain-specific. The changes in the levels of global gene expression due to the response to fluoroquinolone exposure may be governed by complex regulatory processes. Both resistant strains harbored some common and some unique mutations in fluoroquinolone target genes. These enzymes are involved in the DNA supercoiling process that plays an essential role during gene transcription [38, 39]. Although neither of the resistant strains was a clinical isolate, some of the mutations found in the resistant strains were the same as those found in fluoroquinolone-resistant mutants of E. coli MK-1775 in vivo obtained from clinical samples, which were also the same as those
found in fluoroquinolone-resistant mutants of E. coli generated in the laboratory [29, 40]. The expression of a number of genes is affected by supercoiling [19] and aberrant expression of these genes occurs when DNA supercoiling
Reverse transcriptase has been altered by gyrase mutation(s). Alleles of gyrA that reduce DNA supercoiling have been shown to generate metabolic defects and reduce fitness of gyrase mutant strains [38, 41]. Furthermore, TPX-0005 manufacturer because fluoroquinolones are DNA-damaging agents, in addition to inducing mutation in target genes, changing DNA superhelicity, they may also induce the expression of DNA repair genes via the SOS response, which may lead to phenotypic changes [15, 17–20]. Cirz et al. [15] characterized the global transcription response of S. aureus to ciprofloxacin and, among other changes, found induction of the SOS response, upregulation of the TCA cycle and downregulation of α-hemolysin and a leukocidin family toxin. The positive regulators of transcriptional responses for stress and toxin genes were also downregulated [15]. In C. perfringens, although the expression of several virulence genes decreased in one resistant mutant (13124R), it increased in another (NCTRR). The transcription of various genes, including toxin genes, is regulated by virR and virS[32, 42, 43]. VirS is a sensor histidine kinase, which autophosphorylates in response to extracellular signals, and VirR is a response regulator [32, 42, 43]. These two genes, along with vrr (which is an RNA regulator virR-RNA), are implicated in controlling gene transcription [44] and were upregulated in NCTRR. In 13124R, transcription of VirR did not change, and virS and vrr were downregulated.
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