Active Lysogeny in Listeria Monocytogenes Is a Bacteria-Phage Adaptive Response in the Mammalian Environment
Anna Pasechnek,
Lev Rabinovich,
Olga Stadnyuk,
Gil Azulay,
Jessica Mioduser,
Tal Argov,
Ilya Borovok,
Nadejda Sigal,
Anat A. Herskovits
Affiliations
Anna Pasechnek
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel
Lev Rabinovich
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel
Olga Stadnyuk
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel
Gil Azulay
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel
Jessica Mioduser
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel
Tal Argov
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel
Ilya Borovok
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel
Nadejda Sigal
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel
Anat A. Herskovits
The School of Molecular Cell Biology and Biotechnology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel- Aviv 69978, Israel; Corresponding author
Summary: Some Listeria monocytogenes (Lm) strains harbor a prophage within the comK gene, which renders it inactive. During Lm infection of macrophage cells, the prophage turns into a molecular switch, promoting comK gene expression and therefore Lm intracellular growth. During this process, the prophage does not produce infective phages or cause bacterial lysis, suggesting it has acquired an adaptive behavior suited to the pathogenic lifestyle of its host. In this study, we demonstrate that this non-classical phage behavior, named active lysogeny, relies on a transcriptional response that is specific to the intracellular niche. While the prophage undergoes lytic induction, the process is arrested midway, preventing the transcription of the late genes. Further, we demonstrate key phage factors, such as LlgA transcription regulator and a DNA replicase, that support the phage adaptive behavior. This study provides molecular insights into the adaptation of phages to their pathogenic hosts, uncovering unusual cooperative interactions.