Regulation of prophage induction and lysogenization by phage communication systems.
Regulation of prophage induction and lysogenization by phage communication systems.
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DOI：
10.1016/j.cub.2021.08.073
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发表时间：
2021-11-22
期刊：
影响因子：
--
通讯作者：
Gandon S
中科院分区：
文献类型：
--
作者：
Bruce JB;Lion S;Buckling A;Westra ER;Gandon S
许多病毒引起溶解性感染，在那里它们释放病毒颗粒，和休眠感染，在那里它们等待未来的机会重新激活。每种传播模式的益处取决于环境中易感宿主的密度。一些感染细菌的病毒利用分子信号对宿主可用性的变化做出可塑性反应。这些病毒在裂解性感染期间产生信号，并基于环境中的信号浓度来调节它们转变为引起休眠感染的概率。我们提出了一个分析框架，以研究适应性的意义，可塑性在波动的环境中病毒的生活史特征。我们的模型概括和扩展了以前的理论，并预测，主机密度波动应选择可塑性进入溶原性以及一旦信号浓度下降病毒重新激活。使用枯草芽孢杆菌及其噬菌体phi3T，我们实验证实了预测，枯草芽孢杆菌使用信号作出明智的决定超过原噬菌体诱导。我们还表明，溶原细胞产生信号分子和信号被降解的主机在一个密度依赖性的方式。因此，信号浓度下降可能表明存在未感染的宿主并触发原噬菌体诱导。最后，我们发现，溶原化和信号的再激活的反应的冲突是解决通过不同的反应阈值为每个性状的演变。总的来说，这些发现加深了我们对病毒使用分子通讯来调节其感染策略的方式的理解，这些策略可以用来操纵自然环境中的宿主和噬菌体种群动态。噬菌体在溶解和溶原循环期间产生并响应任意信号。信号传递提供了关于易感宿主可用性的间接信息。噬菌体基于该间接信息调节溶原化和再活化。显示了在裂解生长期间和作为原噬菌体时，噬菌体使用分子信号来响应宿主可用性变化。该病毒使用不同的信号响应阈值过渡到溶原性与再活化，允许宿主在易感宿主很多时避免溶原性，而在易感宿主不存在时避免诱导。
Many viruses cause both lytic infections, where they release viral particles, and dormant infections, where they await future opportunities to reactivate. The benefits of each transmission mode depend on the density of susceptible hosts in the environment. Some viruses infecting bacteria use molecular signaling to respond plastically to changes in host availability. These viruses produce a signal during lytic infection and regulate, based on the signal concentration in the environment, the probability with which they switch to causing dormant infections. We present an analytical framework to examine the adaptive significance of plasticity in viral life-history traits in fluctuating environments. Our model generalizes and extends previous theory and predicts that host density fluctuations should select for plasticity in entering lysogeny as well as virus reactivation once signal concentrations decline. Using Bacillus subtilis and its phage phi3T, we experimentally confirm the prediction that phages use signal to make informed decisions over prophage induction. We also demonstrate that lysogens produce signaling molecules and that signal is degraded by hosts in a density-dependent manner. Declining signal concentrations therefore potentially indicate the presence of uninfected hosts and trigger prophage induction. Finally, we find that conflict over the responses of lysogenization and reactivation to signal is resolved through the evolution of different response thresholds for each trait. Collectively, these findings deepen our understanding of the ways viruses use molecular communication to regulate their infection strategies, which can be leveraged to manipulate host and phage population dynamics in natural environments. Phages produce and respond to arbitrium signal during the lytic and lysogenic cycles Signaling provides indirect information on the availability of susceptible hosts Phages adjust lysogenization and reactivation based on this indirect information Phages use distinct signal response thresholds for lysogenization and reactivation Bruce et al. show that phages use molecular signaling to respond to changing host availability during lytic growth and as prophage. The virus uses different signal response thresholds for the transition to lysogeny versus for reactivation, allowing phages to avoid lysogeny when susceptible hosts are many and induction when they are absent.
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影响因子：
6.7
作者：
Berngruber, Thomas W.;Lion, Sebastien;Gandon, Sylvain
通讯作者：
Gandon, Sylvain
影响因子：
6.7
作者：
Rossmann FS;Racek T;Wobser D;Puchalka J;Rabener EM;Reiger M;Hendrickx AP;Diederich AK;Jung K;Klein C;Huebner J
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Huebner J
影响因子：
64.5
作者：
Lazazzera, BA;Solomon, JM;Grossman, AD
通讯作者：
Grossman, AD
影响因子：
4.4
作者：
Altenbuchner, Josef
通讯作者：
Altenbuchner, Josef
影响因子：
64.8
作者：
Erez Z;Steinberger-Levy I;Shamir M;Doron S;Stokar-Avihail A;Peleg Y;Melamed S;Leavitt A;Savidor A;Albeck S;Amitai G;Sorek R
通讯作者：
Sorek R