3 research outputs found
Enhanced antibiotic resistance development from fluoroquinolone persisters after a single exposure to antibiotic
Fluoroquinolone (FQ)-induced DNA damage in persisters could promote antibiotic resistance. Here, using time-lapse microscopy and genetic analyses, the authors show that after a single round of FQ treatment, SOS response in persisters accelerates the development of resistance to unrelated antibiotics
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Development of Persister-FACSeq: a method to massively parallelize quantification of persister physiology and its heterogeneity
Bacterial persisters are thought to underlie the relapse of chronic infections. Knowledge of persister physiology would illuminate avenues for therapeutic intervention; however, such knowledge has remained elusive because persisters have yet to be segregated from other cell types to sufficient purity. This technical hurdle has stymied progress toward understanding persistence. Here we developed Persister-FACSeq, which is a method that uses fluorescence-activated cell sorting, antibiotic tolerance assays, and next generation sequencing to interrogate persister physiology and its heterogeneity. As a proof-of-concept, we used Persister-FACSeq on a library of reporters to study gene expression distributions in non-growing Escherichia coli, and found that persistence to ofloxacin is inversely correlated with the capacity of non-growing cells to synthesize protein. Since Persister-FACSeq can be applied to study persistence to any antibiotic in any environment for any bacteria that can harbor a fluorescent reporter, we anticipate that it will yield unprecedented knowledge of this detrimental phenotype