TRANSLATIONAL RECODING INDUCED BY G-RICH MESSENGER-RNA SEQUENCES THATFORM UNUSUAL STRUCTURES

We investigated a herpesvirus mutant that contains a single base inser tion in its thymidine kinase (tk) gene yet expresses low levels of TK via a net + 1 translational recoding event. Within this mutant gene, w e defined a G-rich signal that is sufficient to induce recoding. Unlik e other translational recoding events, downstream RNA structures or te rmination codons did not stimulate recoding, and paused ribosomes were not detected. Mutational analysis indicated that specific tRNAs or co don-anticodon slippage were unlikely to account for recoding. Rather, recoding efficiency correlated with the G-richness of the signal and i ts ability to form unusual structures. These findings identify a mecha nism of translational recoding with unique features and potential impl ications for clinical drug resistance and other biological systems.