Interactions of the TnaC nascent peptide with rRNA in the exit tunnel enable the ribosome to respond to free tryptophan

Allyson K. Martínez, Emily Gordon, Arnab Sengupta, Nitin Shirole, Dorota Klepacki, Blanca Martinez-Garriga, Lewis M. Brown, Michael Benedik, Charles Yanofsky, Alexander S. Mankin, Nora Vazquez-Laslop, Matthew S. Sachs, Luis R. Cruz-Vera*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)

Abstract

A transcriptional attenuation mechanism regulates expression of the bacterial tnaCAB operon. This mechanism requires ribosomal arrest induced by the regulatory nascent TnaC peptide in response to free L-tryptophan (L-Trp). In this study we demonstrate, using genetic and biochemical analyses, that in Escherichia coli, TnaC residue I19 and 23S rRNA nucleotide A2058 are essential for the ribosome's ability to sense free L-Trp. We show that the mutational change A2058U in 23S rRNA reduces the concentration dependence of L-Trpmediated tna operon induction, whereas the TnaC I19L change suppresses this phenotype, restoring the sensitivity of the translating A2058U mutant ribosome to free L-Trp. These findings suggest that interactions between TnaC residue I19 and 23S rRNA nucleotide A2058 contribute to the creation of a regulatory L-Trp binding site within the translating ribosome.

Original languageEnglish
Pages (from-to)1245-1256
Number of pages12
JournalNucleic Acids Research
Volume42
Issue number2
DOIs
Publication statusPublished - 1 Jan 2014
Externally publishedYes

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