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Mechanism of post-segregational killing: translation of Hok, SrnB and Pnd mRNAs of plasmids R1, F and R483 is activated by 3′-end processing.

1994; Springer Nature; Volume: 13; Issue: 8 Linguagem: Inglês

10.1002/j.1460-2075.1994.tb06464.x

1460-2075

Thomas Thisted, Anne Kirstine Nielsen, Kenn Gerdes,

Genomics and Phylogenetic Studies

Research Article15 April 1994free access Mechanism of post-segregational killing: translation of Hok, SrnB and Pnd mRNAs of plasmids R1, F and R483 is activated by 3′-end processing. T. Thisted T. Thisted Department of Molecular Biology, Odense University, Denmark. Search for more papers by this author A.K. Nielsen A.K. Nielsen Department of Molecular Biology, Odense University, Denmark. Search for more papers by this author K. Gerdes K. Gerdes Department of Molecular Biology, Odense University, Denmark. Search for more papers by this author T. Thisted T. Thisted Department of Molecular Biology, Odense University, Denmark. Search for more papers by this author A.K. Nielsen A.K. Nielsen Department of Molecular Biology, Odense University, Denmark. Search for more papers by this author K. Gerdes K. Gerdes Department of Molecular Biology, Odense University, Denmark. Search for more papers by this author Author Information T. Thisted1, A.K. Nielsen1 and K. Gerdes1 1Department of Molecular Biology, Odense University, Denmark. The EMBO Journal (1994)13:1950-1959https://doi.org/10.1002/j.1460-2075.1994.tb06464.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info The gene systems hok/sok of R1, srnB of F and pnd of R483 mediate plasmid maintenance by killing of plasmid-free segregants. Translation of the very stable mRNAs encoding the killer proteins is regulated by small unstable antisense RNAs. The differential decay rates of the inhibitory antisense RNAs and the mRNAs encoding the killer proteins is the basis for the onset of killer mRNA translation in newborn plasmid-free segregants and the killing of these cells. We have suggested previously that this requires that the killer mRNAs occur in two forms. A translationally inactive form was proposed to be converted into a 3′-truncated, translationally active mRNA. In the presence of the antisense RNA, translation from this killer mRNA should be inhibited. In this communication we present in vivo and in vitro evidence that support this model. The requirement for 3′-processing for killer gene expression is demonstrated. By using in vitro techniques it is shown that full-length Hok mRNA is translationally inactive, whereas a 3′-end truncated version of the Hok mRNA is translationally active. In vitro secondary structure probing suggests that the 3′-end of the full-length Hok mRNA folds back onto the translational initiation region of the mok gene and thereby inhibits translation of the mRNA. By inference we conclude that the Pnd and SrnB mRNAs are regulated by a similar mechanism. Previous ArticleNext Article Volume 13Issue 81 April 1994In this issue RelatedDetailsLoading ...