The human bacterial pathogen Listeria monocytogenes harbors a prophage within its genome, which is known to reproduce by both lytic and lysogenic cycles. We have recently shown that this prophage adopted an unusual behavior when L. monocytogenes infect mammalian cells. During macrophage cells infection the prophage, which is inserted within comK gene, excises its genome leaving an intact comK gene that is necessary to facilitate bacterial phagosomal escape. Prophage excision occurs specifically within phagosomes, yet, unlike classic prophage induction, progeny virions are not produced and bacterial lysis do not occur. These observations insinuated a unique adaptation of the prophage to the intracellular life style of its host, demonstrating a mechanism by which the prophage turn itself into a genetic switch to modulate the virulence of its host1. In the current project we aim to investigate the give-and-take interactions of L. monocytogenes with its prophage during mammalian cells infection and to decipher the molecular mechanisms that control its intracellular excision and maintenance. Searching for phage genes that are specifically induced during macrophage cells infection, reveled several non-coding RNAs as potential regulatory determinants of phage proliferation. Analysis of the transcription profile of these ncRNAs demonstrated that they specifically induced during intracellular infection and not during phage lytic and lysogenic cycles. We are currently exploring the function of these ncRNAs including their down stream regulated genes, preliminary data will be presented.
- Rabinovich et al., Cell 150, 792–802, 2012.
