1887

Abstract

In , the major poly(A) polymerase (PAP I) is encoded by the gene. In this report, a significant impairment of lysogenization by Shiga toxin-converting (Stx) bacteriophages (Φ24, 933W, P22, P27 and P32) is demonstrated in host cells with a mutant gene. Moreover, lytic development of these phages after both infection and prophage induction was significantly less efficient in the mutant than in the WT host. The increase in DNA accumulation of the Stx phages was lower under conditions of defective RNA polyadenylation. Although shortly after prophage induction, the levels of mRNAs of most phage-borne early genes were higher in the mutant, at subsequent phases of the lytic development, a drastically decreased abundance of certain mRNAs, including those derived from the , and genes, was observed in PAP I-deficient cells. All of these effects observed in the cells were significantly more strongly pronounced in the Stx phages than in bacteriophage λ. Abundance of mRNA derived from the gene was drastically increased shortly (20 min) after prophage induction by mitomycin C and decreased after the next 20 min, while no such changes were observed in non-lysogenic cells treated with this antibiotic. This prophage induction-dependent transient increase in transcript may explain the polyadenylation-driven regulation of phage gene expression.

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2015-07-01
2024-04-23
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