The alarming rise in bacterial resilience to antibiotics stems from overuse and misuse. One survival strategy bacteria employ is dormancy, a metabolically quiescent state triggered by the stringent response (SR). The SR is a highly conserved stress signaling pathway used to mitigate the effect of external stressors by shifting gene regulation from active division to dormancy and stress responses within the RpoS regulon. Recently, non-thermal plasma (NTP), partly ionized gas containing ultraviolet (UV) rays, ozone, and charged reactive species, has emerged as a promising alternative to antibiotics. NTP and its multiple effectors have shown to be effective against biofilms -- a major source of these dormant populations -- but the impact of the SR on NTP efficacy is unclear. This study investigates the SR and the RpoS regulon using single-gene knockouts from the Escherichia coli K12 Keio collection. To quantify viable cell populations, we pretreated various E. coli strains with serine hydroxamate (SHX), a known SR inducer, or water, followed by NTP exposure. Colony counts revealed that deleting rpoS and its regulated oxidative stress response gene xthA significantly reduced viable cell counts. Surprisingly, deleting the primary SR gene, relA, increased colony-forming units (CFU) yields in SHX-treated cells exposed to NTP. These findings highlight the critical role of the RpoS regulon and suggest that RelA-independent pathways significantly contribute to reduced NTP susceptibility. This work lays the framework for identifying bacterial responses that may influence the long-term efficacy of NTP.
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Details
Title
Investigating stringent response-mediated tolerance to non-thermal plasma in Escherichia coli
Creators
Lauren Elizabeth Walsh
Contributors
Donald C. Hall Jr. (Advisor) - Drexel University, Microbiology and Immunology
Vandana Miller (Advisor)
Awarding Institution
Drexel University
Degree Awarded
Master of Science (M.S.)
Publisher
Drexel University; Philadelphia, Pennsylvania
Number of pages
vii, 42 pages
Resource Type
Thesis
Language
English
Academic Unit
Microbiology and Immunology; College of Medicine; Drexel University
Other Identifier
991022072695204721
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