Open AccessA novel 3′-end repair mechanism in an RNA virus
Author(s) -
Peter D. Nagy,
Clifford D. Carpenter,
Anne Simon
Publication year - 1997
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.94.4.1113
Subject(s) - rna , biology , rna dependent rna polymerase , microbiology and biotechnology , non coding rna , small nuclear rna , rna editing , base pair , genetics , dna , gene
Many positive-stranded RNA viruses contain short, single-stranded 3′ ends that are vulnerable to degradation by host cellular RNases. Therefore, the existence of a 3′-end repair mechanism (analogous to cellular telomerases) must be required and/or advantageous for RNA viruses. Accordingly, we provide evidence suggesting that deletions of up to 6 nt from the 3′ end of satellite (sat-) RNA C (a small parasitic RNA associated with turnip crinkle carmovirus) are repaired to the wild-type sequencein vivo andin vitro . The novel 3′-end repair mechanism involves the production of 4–8 nt oligoribonucleotides by abortive synthesis by the viral replicase using the 3′ end of the viral genomic RNA as template. Based on ourin vitro results, we postulate that the oligoribonucleotides are able to prime synthesis of wild-type negative-strand sat-RNA C in a reaction that does not require base pairing of the oligoribonucleotides to the mutant, positive-strand RNA template. The discovery of a 3′-end repair mechanism opens up new strategies for interfering with viral infections.