Ichikawa Shunsuke, Tanoue Midai, Takeuchi Junto, Matsuo Eri, Shimada Yasuhito, Singh Abhyudai
Faculty of Education, Mie University, 1577 Kurimamachiya-cho Tsu, Mie, 514-8507, Japan.
Zebrafish Research Center, Mie University, 1577 Kurimamachiya-cho Tsu, Mie, 514-8507, Japan.
bioRxiv. 2025 May 15:2025.05.14.654146. doi: 10.1101/2025.05.14.654146.
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 . 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 indicate that survives UV stress via an induced, rather than pre-existing, mechanism of tolerance.
瞬时耐受细菌亚群的出现挑战了我们对胁迫耐受机制的理解。虽然我们对抗生素耐受性了解很多，但尚不清楚类似机制是否有助于在紫外线（UV）胁迫下存活。在这里，我们采用改良的卢里亚-德尔布吕克波动试验来研究[具体对象]中预先存在的耐紫外线亚群的存在情况。我们的结果没有显示出应激前紫外线耐受性的显著证据。相反，数据表明存活主要由紫外线暴露后激活的诱导性DNA修复反应驱动。此外，连续低剂量紫外线暴露产生了高于预期的存活率，这表明在初始紫外线暴露后可能通过活跃的DNA修复过程诱导产生瞬时耐受性。这些发现表明，[具体对象]通过诱导而非预先存在的耐受机制在紫外线胁迫下存活。
