Rex-Centric Mutualism

Department of Microbiology and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E5, Canada.
Journal of Bacteriology (Impact Factor: 2.81). 03/2002; 184(3):857-8. DOI: 10.1128/JB.184.3.857-858.2002
Source: PubMed


We asked whether Rex exclusion encoded by a lambda prophage confers a protective or a cell-killing phenotype. We found that
the Rex system can channel lysogenic cells into an arrested growth phase that gives an overall protective ability to the host
despite some associated killing.

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Available from: Roderick A Slavcev, Jan 24, 2014
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    • "Some constitutive independent expression of rexB from p Lit must occur in a lysogenic prophage, since a p M -defective prophage in double lysogens [(cI857 p M 116)(gal8 rex-cI857 cII68)] or [(cI857 p M E37)(gal8 rex-cI857 cII68)] can complement for rexB mutations, but not for rexA mutations (Matz et al. 1982). Rex exclusion, encoded by genes rexA and rexB (Matz et al. 1982; Landsman et al. 1982), can prevent the lytic growth of several bacteriophages that infect lysogens (Shinedling et al. 1987; Toothman and Herskowitz 1980a; Slavcev and Hayes 2002). Slavcev and Hayes (2003a) found that the degree to which Rex + host cells survived a T4rII infection depended upon an activity of the host stationary-phase sigma factor RpoS. "
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    ABSTRACT: The cI-rexA-rexB operon of bacteriophage lambda confers 2 phenotypes, Imm and Rex, to lysogenic cells. Immunity to homoimmune infecting lambda phage depends upon the CI repressor. Rex exclusion of T4rII mutants requires RexA and RexB proteins. Both Imm and Rex share temperature-sensitive conditional phenotypes when expressed from cI[Ts]857 but not from cI+ lambda prophage. Plasmids were made in which cI-rexA-rexB was transcribed from a non-lambda promoter, pTet. The cI857-rexA-rexB plasmid exhibited Ts conditional Rex and CI phenotypes; the cI+-rexA-rexB plasmid did not. Polarity was observed within cI-rexA-rexB transcription at sites in cI and rexA when CI was nonfunctional. Renaturation of the Ts CI857 repressor, allowing it to regain functionality, suppressed the polar effect on downstream transcription from the site in cI. The second strong polar effect near the distal end of rexA was observed for transcription initiated from pE. The introduction of a rho Ts mutation into the host genome suppressed both polar effects, as measured by its suppression of the conditional Rex phenotype. Strong suppression of the conditional Rex[Ts] phenotype was imparted by ssrA and clpP (polar for clpX) null mutations, suggesting that RexA or RexB proteins made under conditions of polarity are subject to 10Sa RNA tagging and ClpXP degradation.
    Full-text · Article · Feb 2005 · Canadian Journal of Microbiology
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    ABSTRACT: The rex genes of bacteriophage lambda were found to protect lysogenic Escherichia coliK host cells against killing by phage T4 rII, when compared in parallel to isogenic Rex(-) lysogens and nonlysogens. This protective effect was abrogated upon mutation of the host stationary-phase sigma factor RpoS. Rex(+) lysogens infected by T4 rII contracted, formed aggregates and shed flagella, thus resembling cells entering stationary phase. These phenotypes were accentuated in nonlysogenic cells carrying multicopy plasmids expressing rexA-rexB: cells were about two-fold contracted in length, expressed membrane-bound and detached flagella, were insensitive to infection by a variety of phages and clumped extensively; in addition, cultures of these cells were odorous. Our observations support the hypothesis that the Rex system can cause a stationary-phase-like response that protects the host against infection by T4 rII.
    No preview · Article · May 2003 · Molecular Genetics and Genomics
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    ABSTRACT: Dosage and relative cellular levels of RexA and RexB proteins encoded by the rexA-rexB genes of a lambda prophage are important for the Rex+ phenotype, which was nullified when greater RexA or RexB was provided than was necessary for the complementation of a rexA- or a rexB- prophage.
    No preview · Article · Mar 2004 · Canadian Journal of Microbiology
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