Translational recoding induced by G-rich mRNA sequences that form unusual structures.

Abstract:

:We investigated a herpesvirus mutant that contains a single base insertion in its thymidine kinase (tk) gene yet expresses low levels of TK via a net +1 translational recoding event. Within this mutant gene, we defined a G-rich signal that is sufficient to induce recoding. Unlike other translational recoding events, downstream RNA structures or termination codons did not stimulate recoding, and paused ribosomes were not detected. Mutational analysis indicated that specific tRNAs or codon-anticodon slippage were unlikely to account for recoding. Rather, recoding efficiency correlated with the G-richness of the signal and its ability to form unusual structures. These findings identify a mechanism of translational recoding with unique features and potential implications for clinical drug resistance and other biological systems.

journal_name

Cell

journal_title

Cell

authors

Horsburgh BC,Kollmus H,Hauser H,Coen DM

doi

10.1016/s0092-8674(00)80170-1

subject

Has Abstract

pub_date

1996-09-20 00:00:00

pages

949-59

issue

6

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(00)80170-1

journal_volume

86

pub_type

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