AI Insight
When bacteriophages infect a bacterial cell, they face a fundamental decision: replicate and destroy the host (lysis) or integrate into the host genome and coexist (lysogeny). This decision is influenced by the multiplicity of infection (MOI), meaning the number of phage particles infecting a single cell. The authors present a minimal mathematical model demonstrating that only a limited set of molecular mechanisms, such as host proteases, kinases, or RNases acting asymmetrically on one of the two pathways, can account for how phages sense and respond to MOI to make this regulatory choice.
Why it matters
Understanding how phages switch between lysis and lysogeny has implications for phage therapy, bacterial genome evolution, and the control of bacterial populations in clinical and environmental contexts. This modeling framework may also help predict phage behavior in complex microbial communities where infection dynamics vary.
⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Upon infecting a bacterium, temperate phages must decide between killing the cell to reproduce (lysis) or entering a symbiotic lifestyle (lysogeny). This choice is often informed by the cell’s state, as well as the number of infecting phage particles (MOI). Since phage gene copy numbers scale identically with MOI, an MOI-dependent decision requires a fast-acting asymmetry between the lytic and lysogenic pathways. We introduce a minimal model suggesting that only a handful of coupling mechanisms can produce such an asymmetry; for instance via a host protease, kinase, or RNase acting on one pathway. By distilling complex regulatory networks to their essential components, our model clarifies the logic of lysis-lysogeny decision mechanisms across phage species.
Source: Counting to two: how phages decide between lysis and lysogeny