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An antisense RNA inhibits translation by competing with standby ribosomes
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Cell and Molecular Biology, Microbiology. (Wagner)
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Cell and Molecular Biology, Microbiology. (Wagner)
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Cell and Molecular Biology, Microbiology. (Wagner)
2007 (English)In: Molecular Cell, ISSN 1097-2765, E-ISSN 1097-4164, Vol. 26, no 3, 381-392 p.Article in journal (Refereed) Published
Abstract [en]

Most antisense RNAs in bacteria inhibit translation by competing with ribosomes for translation initiation regions (TIRs) on nascent mRNA. We propose a mechanism by which an antisense RNA inhibits translation without binding directly to a TIR. The tisAB locus encodes an SOS-induced toxin, and IstR-1 is the antisense RNA that counteracts toxicity. We show that full-length tisAB mRNA (+1) is translationally inactive and endonucleolytic processing produces an active mRNA (+42). IstR-1 binding inhibits translation of this mRNA, and subsequent RNase III cleavage generates a truncated, inactive mRNA (+106). In vitro translation, toeprinting, and structure mapping suggest that active, but not inactive, tisAB mRNAs contain an upstream ribosome loading or “standby” site. Standby binding is required for initiation at the highly structured tisB TIR. This may involve ribosome sliding to a transiently open tisB TIR. IstR-1 competes with ribosomes by base pairing to the standby site located 100 nucleotides upstream.

Place, publisher, year, edition, pages
2007. Vol. 26, no 3, 381-392 p.
Keyword [en]
RNA
National Category
Biological Sciences
Identifiers
URN: urn:nbn:se:uu:diva-12967DOI: 10.1016/j.molcel.2007.04.003ISI: 000246666700006PubMedID: 17499044OAI: oai:DiVA.org:uu-12967DiVA: diva2:40737
Available from: 2008-05-29 Created: 2008-05-29 Last updated: 2017-12-11Bibliographically approved

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Wagner, Gerhart E. H.

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