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Uneven host cell growth causes lysogenic virus induction in the Baltic Sea

机译:宿主细胞生长不均会在波罗的海引起溶源性病毒诱导

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摘要

In the Baltic Sea redoxcline, lysogenic viruses infecting prokaryotes have rarely been detected using the commonly used inducing agent mitomycin C. However, it is well known that not all viruses are induceable by mitomycin C and growing evidence suggests that changes in trophic conditions may trigger the induction of lysogenic viruses. We hypothesized that using antibiotics to simulate a strong change in trophic conditions for antibiotica-resistant cells due to reduced competition for resources might lead to the induction of lysogenic viruses into the lytic cycle within these cells. This hypothesis was tested by incubating prokaryotes obtained throughout the Baltic Sea redoxcline in seawater with substantially reduced numbers of viruses. We used a mixture of the protein synthesis-inhibiting antibiotics streptomycin and erythromycin to induce the desired changes in trophic conditions for resistant cells and at the same time ensuring that no progeny viruses were formed in sensitive cells. No inducible lysogenic viruses could be detected in incubations amended with mitomycin C. Yet, the presence of streptomycin and erythromycin increased virus-induced mortality of prokaryotes by 56–930% compared to controls, resulting in the induction of lysogenic viruses equivalent to 2–14% of in situ prokaryotic abundance. The results indicate the existence of a previously unrecognized induction mechanism for lysogenic viruses in the Baltic Sea redoxcline, as the mode of action distinctly differs between the used antibiotics (no virus production within affected cells) and mitomycin C (lysogenic viruses are produced within affected cells). Obtaining accurate experimental data on levels of lysogeny in prokaryotic host cells remains challenging, as relying on mitomycin C alone may severely underestimate lysogeny.
机译:在波罗的海氧化还原菌中,很少使用常用的诱导剂丝裂霉素C检测到感染原核生物的溶原性病毒。但是,众所周知,并非所有病毒都能被丝裂霉素C诱导,并且越来越多的证据表明营养条件的改变可能会触发丝裂霉素C。溶源性病毒的诱导。我们假设由于对资源的竞争减少而使用抗生素模拟抗药性细胞营养状况的强烈变化,可能会导致溶原性病毒诱导进入这些细胞的裂解周期。通过在整个波罗的海氧化还原细胞中将原核生物与病毒数量显着减少的海水一起温育来检验该假设。我们使用了抑制蛋白质合成的抗生素链霉素和红霉素的混合物,以诱导抗性细胞营养状况发生所需的变化,同时确保在敏感细胞中不形成子代病毒。用丝裂霉素C修饰的培养液中未检测到可诱导的溶原性病毒。但是,链霉素和红霉素的存在与对照组相比,原核生物的病毒诱导死亡率增加了56–930%,导致诱导了2–14的溶原性病毒原位原核丰度的百分比。结果表明在波罗的海氧化还原细胞中存在溶血原性病毒的一种先前无法识别的诱导机制,因为所用抗生素(受影响的细胞内无病毒产生)和丝裂霉素C(受影响的细胞内产生溶源性病毒)之间的作用方式明显不同)。获得准确的原核宿主细胞溶血原水平的实验数据仍然具有挑战性,因为仅依靠丝裂霉素C可能会严重低估溶血原。

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