Scholarlink

<p>The emergence of transiently tolerant bacterial subpopulations challenges our understanding of stress tolerance mechanisms. While much is known about antibiotic tolerance, it remains unclear whether similar mechanisms contribute to survival under ultraviolet (UV) stress. Here, we employed a modified Luria–Delbrück fluctuation test to investigate the presence of pre-existing UV-tolerant subpopulations in <i>Escherichia coli</i>. Our results showed no significant evidence of pre-stress UV tolerance. Instead, the data suggest that survival is primarily driven by inducible DNA repair responses activated after UV exposure. Furthermore, sequential low-dose UV exposures yielded higher-than-expected survival, suggesting that transient tolerance can be induced following initial UV exposure, likely through active DNA repair processes. These findings suggest that <i>E. coli</i> survival under UV stress is more consistent with an induced, rather than pre-existing, mechanism of tolerance.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Induced tolerance to UV stress drives survival heterogeneity in isogenic E. coli cell populations

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月21日

查看全文
  • Shunsuke Ichikawa,
  • Midai Tanoue,
  • Junto Takeuchi,
  • Takuto Fujitani,
  • Mizuki Goto,
  • Rise Sanda,
  • Eri Matsuo,
  • Yasuhito Shimada,
  • Abhyudai Singh

摘要

The emergence of transiently tolerant bacterial subpopulations challenges our understanding of stress tolerance mechanisms. While much is known about antibiotic tolerance, it remains unclear whether similar mechanisms contribute to survival under ultraviolet (UV) stress. Here, we employed a modified Luria–Delbrück fluctuation test to investigate the presence of pre-existing UV-tolerant subpopulations in Escherichia coli. Our results showed no significant evidence of pre-stress UV tolerance. Instead, the data suggest that survival is primarily driven by inducible DNA repair responses activated after UV exposure. Furthermore, sequential low-dose UV exposures yielded higher-than-expected survival, suggesting that transient tolerance can be induced following initial UV exposure, likely through active DNA repair processes. These findings suggest that E. coli survival under UV stress is more consistent with an induced, rather than pre-existing, mechanism of tolerance.