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Personne :
Samson, Julie

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Samson

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Julie

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Département de biochimie, microbiologie et bio-informatique, Faculté des sciences et de génie, Université Laval

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ncf12004035

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Voici les éléments 1 - 4 sur 4
  • PublicationRestreint
    Lactococcal abortive infection protein AbiV interacts directly with the phage protein SaV and prevents translation of phage proteins
    (American Society for Microbiology, 2010-10-25) Haaber, Jakob; Moineau, Sylvain; Labrie, Simon; Samson, Julie; Campanacci, Valérie; Cambillau, Christian; Hammer, Karin
    AbiV is an abortive infection protein that inhibits the lytic cycle of several virulent phages infecting Lactococcus lactis, while a mutation in the phage gene sav confers insensitivity to AbiV. In this study, we have further characterized the effects of the bacterial AbiV and its interaction with the phage p2 protein SaV. First, we showed that during phage infection of lactococcal AbiV+ cells, AbiV rapidly inhibited protein synthesis. Among early phage transcripts, sav gene transcription was slightly inhibited while the SaV protein could not be detected. Analyses of other phage p2 mRNAs and proteins suggested that AbiV blocks the activation of late gene transcription, probably by a general inhibition of translation. Using size exclusion chromatography coupled with on-line static light scattering and refractometry, as well as fluorescence quenching experiments, we also demonstrated that both AbiV and SaV formed homodimers and that they strongly and specifically interact with each other to form a stable protein complex.
  • PublicationAccès libre
    Lactococcal abortive infection protein AbiV interacts directly with the phage protein SaV and prevents translation of phage proteins
    (American Society for Microbiology, 2010-10-25) Haaber, Jakob; Moineau, Sylvain; Labrie, Simon; Samson, Julie; Campanacci, Valérie; Cambillau, Christian; Hammer, Karin
    AbiV is an abortive infection protein that inhibits the lytic cycle of several virulent phages infecting Lactococcus lactis, while a mutation in the phage gene sav confers insensitivity to AbiV. In this study, we have further characterized the effects of the bacterial AbiV and its interaction with the phage p2 protein SaV. First, we showed that during phage infection of lactococcal AbiV cells, AbiV rapidly inhibited protein synthesis. Among early phage transcripts, sav gene transcription was slightly inhibited while the SaV protein could not be detected. Analyses of other phage p2 mRNAs and proteins suggested that AbiV blocks the activation of late gene transcription, probably by a general inhibition of translation. Using size exclusion chromatography coupled with on-line static light scattering and refractometry, as well as fluorescence quenching experiments, we also demonstrated that both AbiV and SaV formed homodimers and that they strongly and specifically interact with each other to form a stable protein complex.
  • PublicationRestreint
    Bacteriophage resistance mechanisms
    (Nature Publishing Group, 2010-03-29) Moineau, Sylvain; Labrie, Simon; Samson, Julie
    Phages are now acknowledged as the most abundant microorganisms on the planet and are also possibly the most diversified. This diversity is mostly driven by their dynamic adaptation when facing selective pressure such as phage resistance mechanisms, which are widespread in bacterial hosts. When infecting bacterial cells, phages face a range of antiviral mechanisms, and they have evolved multiple tactics to avoid, circumvent or subvert these mechanisms in order to thrive in most environments. In this Review, we highlight the most important antiviral mechanisms of bacteria as well as the counter-attacks used by phages to evade these systems.
  • PublicationRestreint
    Bacteriophage resistance mechanisms
    (Nature Pub. Group, 2010-03-29) Moineau, Sylvain; Labrie, Simon; Samson, Julie
    Phages are now acknowledged as the most abundant microorganisms on the planet and are also possibly the most diversified. This diversity is mostly driven by their dynamic adaptation when facing selective pressure such as phage resistance mechanisms, which are widespread in bacterial hosts. When infecting bacterial cells, phages face a range of antiviral mechanisms, and they have evolved multiple tactics to avoid, circumvent or subvert these mechanisms in order to thrive in most environments. In this Review, we highlight the most important antiviral mechanisms of bacteria as well as the counter-attacks used by phages to evade these systems.