摘要
杀手酵母（如 S. Cerevisiae 的 K1 杀手菌株）表达一种分泌型反竞争毒素，这种毒素的产生和传播需要两种垂直传播的 dsRNA 病毒的存在。在缺乏杀手病毒感染的敏感细胞中，毒素与细胞壁的结合会导致离子孔的形成、渗透平衡的破坏和细胞的死亡。然而，K1 毒素杀伤活性的确切机制、杀手酵母如何对自身毒素产生免疫以及哪些因素会影响以前敏感种群对 K1 毒素的适应性和抵抗力，这些问题仍然不得而知。在此，我们将介绍有关 K1 杀人酵母毒素的知识现状，包括毒素处理和杀伤活性的现有模型，以及 K1 毒素免疫和抗性的已知调节因子摘要。此外，我们还讨论了两个关键的信号通路，即 HOG（高渗透压甘油）和 CWI（细胞壁完整性），这些通路参与敏感细胞对 K1 杀手毒素的适应性反应的情况以前已有记载，但还需要进一步研究。由于在 K1 等杀手系统中已经记录了宿主-病毒和敏感-杀手之间的竞争，对 K1 杀手酵母的进一步鉴定可能会为研究细胞内遗传冲突以及竞争的敏感和杀手种群之间的反适应提供一个有用的模型系统。Killer yeasts, such as the K1 killer strain of S. Cerevisiae, express a secreted anti-competitive toxin whose production and propagation require the presence of two vertically-transmitted dsRNA viruses. In sensitive cells lacking killer virus infection, toxin binding to the cell wall results in ion pore formation, disruption of osmotic homeostasis, and cell death. However, the exact mechanism(s) of K1 toxin killing activity, how killer yeasts are immune to their own toxin, and which factors could influence adaptation and resistance to K1 toxin within formerly sensitive populations are still unknown. Here, we describe the state of knowledge about K1 killer toxin, including current models of toxin processing and killing activity, and a summary of known modifiers of K1 toxin immunity and resistance. In addition, we discuss two key signaling pathways, HOG (high osmolarity glycerol) and CWI (cell wall integrity), whose involvement in an adaptive response to K1 killer toxin in sensitive cells has been previously documented but requires further study. As both host-virus and sensitive-killer competition have been documented in killer systems like K1, further characterization of K1 killer yeasts may provide a useful model system for study of both intracellular genetic conflict and counter-adaptation between competing sensitive and killer populations.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
