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Quantification of Lysogeny Caused by Phage Coinfections in Microbial Communities from Biophysical Principles.
mSystems ( IF 6.4 ) Pub Date : 2020-09-15 , DOI: 10.1128/msystems.00353-20
Antoni Luque 1, 2, 3 , Cynthia B Silveira 4
Affiliation  

Temperate phages can associate with their bacterial host to form a lysogen, often modifying the phenotype of the host. Lysogens are dominant in the microbially dense environment of the mammalian gut. This observation contrasts with the long-standing hypothesis of lysogeny being favored at low microbial densities, such as in oligotrophic marine environments. Here, we hypothesized that phage coinfections—a well-understood molecular mechanism of lysogenization—increase at high microbial abundances. To test this hypothesis, we developed a biophysical model of coinfection for marine and gut microbiomes. The model stochastically sampled ranges of phage and bacterial concentrations, adsorption rates, lysogenic commitment times, and community diversity from each environment. In 90% of the sampled marine communities, less than 10% of the bacteria were predicted to be lysogenized via coinfection. In contrast, 25% of the sampled gut communities displayed more than 25% of lysogenization. The probability of lysogenization in the gut was a consequence of the higher densities and higher adsorption rates. These results suggest that, on average, coinfections can form two trillion lysogens in the human gut every day. In marine microbiomes, which were characterized by lower densities and phage adsorption rates, lysogeny via coinfection was still possible for communities with long lysogenic commitment times. Our study indicates that different physical factors causing coinfections can reconcile the traditional view of lysogeny at poor host growth (long commitment times) and the recent Piggyback-the-Winner framework proposing that lysogeny is favored in rich environments (high densities and adsorption rates).

中文翻译:

从生物物理原理量化微生物群落中噬菌体共感染引起的溶原性。

温带噬菌体可以与它们的细菌宿主结合形成溶原菌,通常会改变宿主的表型。溶原菌在哺乳动物肠道微生物密集的环境中占主导地位。这一观察结果与溶原性在低微生物密度下受到青睐的长期假设形成对比,例如在贫营养海洋环境中。在这里,我们假设噬菌体共感染——一种众所周知的溶原化分子机制——在高微生物丰度下增加。为了验证这一假设,我们开发了一种海洋和肠道微生物组共感染的生物物理模型。该模型从每个环境中随机采样噬菌体和细菌浓度、吸附率、溶原性承诺时间和群落多样性的范围。在 90% 的采样海洋群落中,预计不到 10% 的细菌会通过共感染溶原化。相比之下,25% 的采样肠道群落表现出超过 25% 的溶原化。肠道中溶原化的可能性是更高密度和更高吸附率的结果。这些结果表明,平均而言,合并感染每天可以在人类肠道中形成 2 万亿个溶原菌。在以较低密度和噬菌体吸附率为特征的海洋微生物组中,对于溶原性定型时间较长的群落,通过共感染进行溶原性仍然是可能的。
更新日期:2020-09-15
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