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
Celljournal_title
Cellauthors
Horsburgh BC,Kollmus H,Hauser H,Coen DMdoi
10.1016/s0092-8674(00)80170-1subject
Has Abstractpub_date
1996-09-20 00:00:00pages
949-59issue
6eissn
0092-8674issn
1097-4172pii
S0092-8674(00)80170-1journal_volume
86pub_type
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