State Key Laboratory of Tea Plant Biology and Utilization, School of Tea and Food Sciences and Technology, Anhui Agricultural University, Hefei, 230036, People's Republic of China.
Key Laboratory of Bioresource and Environmental Biotechnology of Anhui Higher Education Institutes, School of Bioengineering, Huainan Normal University, Huainan, 232001, People's Republic of China.
Sci Rep. 2023 Feb 24;13(1):3225. doi: 10.1038/s41598-022-26554-8.
Our research group has recently found that radiation-induced airborne stress signals can be used for communication among Caenorhabditis elegans (C. elegans). This paper addresses the question of whether heat stress can also induce the emission of airborne stress signals to alert neighboring C. elegans and elicit their subsequent stress response. Here, we report that heat-stressed C. elegans produces volatile stress signals that trigger an increase in radiation resistance in neighboring unheated C. elegans. When several loss-of-function mutations affecting thermosensory neuron (AFD), heat shock factor-1, HSP-4, and small heat-shock proteins were used to test heat-stressed C. elegans, we found that the production of volatile stress signals was blocked, demonstrating that the heat shock response and ER pathway are involved in controlling the production of volatile stress signals. Our data further indicated that mutations affecting the DNA damage response (DDR) also inhibited the increase in radiation resistance in neighboring unheated C. elegans that might have received volatile stress signals, indicating that the DDR might contribute to radioadaptive responses induction by volatile stress signals. In addition, the regulatory pattern of signal production and action was preliminarily clarified. Together, the results of this study demonstrated that heat-stressed nematodes communicate with unheated nematodes via volatile stress signals.
我们的研究小组最近发现，辐射诱导的空气传播应激信号可用于秀丽隐杆线虫（C. elegans）之间的通信。本文探讨了热应激是否也能诱导空气传播应激信号的释放，以警告邻近的 C. elegans 并引发其随后的应激反应。在这里，我们报告称，受热胁迫的 C. elegans 会产生挥发性应激信号，从而提高邻近未受热的 C. elegans 的辐射抗性。当使用几种影响热敏神经元（AFD）、热休克因子 1、HSP-4 和小热休克蛋白的功能丧失突变来测试受热胁迫的 C. elegans 时，我们发现挥发性应激信号的产生被阻断，表明热休克反应和内质网途径参与控制挥发性应激信号的产生。我们的数据进一步表明，影响 DNA 损伤反应（DDR）的突变也抑制了邻近未受热的 C. elegans 中辐射抗性的增加，这些 C. elegans 可能已经接收到挥发性应激信号，表明 DDR 可能有助于由挥发性应激信号诱导的辐射适应性反应。此外，还初步阐明了信号产生和作用的调控模式。总之，这项研究的结果表明，受热胁迫的线虫通过挥发性应激信号与未受热的线虫进行通信。
