| Autor: |
Peltz, Stuart W., Hammell, Amy B., Cui, Ying, Yasenchak, Jason, Puljanowski, Lara, Dinman, Jonathan D. |
| Zdroj: |
Molecular and Cellular Biology; January 1999, Vol. 19 Issue: 1 p384-391, 8p |
| Abstrakt: |
ABSTRACTProgrammed -1 ribosomal frameshifting is utilized by a number of RNA viruses as a means of ensuring the correct ratio of viral structural to enzymatic proteins available for viral particle assembly. Altering frameshifting efficiencies upsets this ratio, interfering with virus propagation. We have previously demonstrated that compounds that alter the kinetics of the peptidyl-transfer reaction affect programmed -1 ribosomal frameshift efficiencies and interfere with viral propagation in yeast. Here, the use of a genetic approach lends further support to the hypothesis that alterations affecting the ribosome’s peptidyltransferase activity lead to changes in frameshifting efficiency and virus loss. Mutations in theRPL3gene, which encodes a ribosomal protein located at the peptidyltransferase center, promote approximately three- to fourfold increases in programmed -1 ribosomal frameshift efficiencies and loss of the M1killer virus of yeast. Themak8-1allele of RPL3contains two adjacent missense mutations which are predicted to structurally alter the Mak8-1p. Furthermore, a second allele that encodes the N-terminal 100 amino acids of L3 (called L3?) exerts atrans-dominant effect on programmed -1 ribosomal frameshifting and killer virus maintenance. Taken together, these results support the hypothesis that alterations in the peptidyltransferase center affect programmed -1 ribosomal frameshifting. |
| Databáze: |
Supplemental Index |
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