Molecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California, USA.
Molecular and Computational Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California, USA
Appl Environ Microbiol. 2019 Jan 9;85(2). doi: 10.1128/AEM.02113-18. Print 2019 Jan 15.
When K-12 is inoculated into rich medium in batch culture, cells experience five phases. While the lag and logarithmic phases are mechanistically fairly well defined, the stationary phase, death phase, and long-term stationary phase are less well understood. Here, we characterize a mechanism of delaying death, a phenomenon we call the "alcohol effect," where the addition of small amounts of certain alcohols prolongs stationary phase for at least 10 days longer than in untreated conditions. We show that the stationary phase is extended when ethanol is added above a minimum threshold concentration. Once ethanol levels fall below a threshold concentration, cells enter the death phase. We also show that the effect is conferred by the addition of straight-chain alcohols 1-propanol, 1-butanol, 1-pentanol, and, to a lesser degree, 1-hexanol. However, methanol, isopropanol, 1-heptanol, and 1-octanol do not delay entry into death phase. Though modulated by RpoS, the alcohol effect does not require RpoS activity or the activities of the AdhE or AdhP alcohol dehydrogenases. Further, we show that ethanol is capable of extending the life span of stationary-phase cultures for non-K-12 strains and that this effect is caused in part by genes of the glycolate degradation pathway. These data suggest a model where ethanol and other shorter 1-alcohols can serve as signaling molecules, perhaps by modulating patterns of gene expression that normally regulate the transition from stationary phase to death phase. In one of the most well-studied organisms in the life sciences, , we still do not fully understand what causes populations to die. This is largely due to the technological difficulties of studying bacterial cell death. This study provides an avenue to studying how and why populations, and perhaps other microbes, transition from stationary phase to death phase by exploring how ethanol and other alcohols delay the onset of death. Here, we demonstrate that alcohols are acting as signaling molecules to achieve the delay in death phase. This study not only offers a better understanding of a fundamental process but perhaps also provides a gateway to studying the dynamics between ethanol and microbes in the human gastrointestinal tract.
当 K-12 在分批培养中接种到丰富的培养基中时，细胞会经历五个阶段。虽然滞后和对数期在机制上已经相当明确，但静止期、死亡期和长期静止期的理解较少。在这里，我们描述了一种延迟死亡的机制，我们称之为“酒精效应”，即在未处理条件下，添加少量某些醇类可将静止期延长至少 10 天。我们表明，当添加的乙醇超过最小阈值浓度时，静止期会延长。一旦乙醇水平降至阈值浓度以下，细胞就会进入死亡期。我们还表明，这种效应是通过添加直链醇 1-丙醇、1-丁醇、1-戊醇和在较小程度上的 1-己醇来实现的。然而，甲醇、异丙醇、1-庚醇和 1-辛醇不会延迟进入死亡期。尽管受 RpoS 调节，但酒精效应不需要 RpoS 活性或 AdhE 或 AdhP 醇脱氢酶的活性。此外，我们表明乙醇能够延长非 K-12 菌株的静止期培养物的寿命，并且这种效应部分是由乙醛酸降解途径的基因引起的。这些数据表明，乙醇和其他较短的 1-醇可以作为信号分子，可能通过调节通常调节从静止期到死亡期的过渡的基因表达模式。在生命科学中研究最深入的生物体之一中，我们仍然不完全了解是什么导致种群死亡。这在很大程度上是由于研究细菌细胞死亡的技术困难。本研究提供了一种通过探索乙醇和其他醇类如何延迟死亡期的发生来研究为什么和为什么 K-12 种群以及其他微生物从静止期过渡到死亡期的途径。在这里，我们证明醇类是通过作为信号分子来实现延迟死亡期的。这项研究不仅提供了对基本过程的更好理解，而且可能为研究乙醇和微生物在人类胃肠道中的动态关系提供了一个途径。
