Nature research paper: Small protein modules dictate prophage fates during polylysogeny
activates the transcription of a counter-oriented gene called. Production of Qtip induces host-cell lysis. Our hypothesis is that through the surveillance of a bacterial-produced QS signal, the phage can integrate host-cell density information into its decision-making process. Moreover, by lysing its host at high cell density, the phage maximizes the probability of infecting other cells in the population.
Bacteria commonly harbour multiple prophages, a state called polylysogeny. How prophages residing in a polylysogenic host compete for host resources is not well understood. What is known is that following DNA damage, the number of virions released for lambdoid prophages is lower in polylysogens than in monolysogens. This result suggests that in polylysogens, co-induced prophages compete for reproductive success.
The current work describes the discovery of SOS-independent, phage-encoded lysis-inducing modules that, despite bearing little resemblance to one another at the sequence level, share a common regulatory logic. Our characterization of several of these phages shows that they all use a transcription factor to activate the expression of a divergently transcribed gene encoding a small protein . The smORF induces the transition from lysogeny to lysis.
The prophage-containing isolates on which we focus are polylysogenic. We show that the addition of a DNA-damaging agent leads to phage-mediated lysis of the bacteria and the release of a mixed population of phage particles. Single-cell analyses demonstrate that this outcome stems from a subset of host cells expressing lytic genes from only one of the phages, another subset expressing lytic genes from only the other phage and the final subset of cells expressing lytic genes from both phages.
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