[Natural UAG suppressor glutamine tRNA in retrovirus infected cells].
Mammalian cells contain two species of glutamine tRNAs, tRNA(CUGGIn) and tRNA(UmUGGIn). The later minor glutamine tRNA which has the UmUG anticodon sequence can recognize an UAG amber termination codon of natural mRNA in an in vitro translation system. Recognition of the UAG nonsense codon by mammalian tRNA(UmUGGIn) is facilitated by two wobble base-pairs at the first and third position of the anticodon. Such unorthodox interaction between the codon and the anticodon which is not in accordance with the wobble hypothesis or the two out of three reading mechanism has been shown only in the recognition of the UAG nonsense codon by natural suppressor tRNA such as yeast tRNA(SGIn) and bovine liver tRNA(CAGLeu). Due to such unique interaction with mRNA, the suppressor activity of mammalian glutamine tRNA(UmUGGIn) is weaker than that of tobacco tRNA(G psi ATyr), which is known to be a natural UAG suppressor tRNA in plants. Retrovirus infection followed by vegetative growth causes the selective and remarkable increase of the amount of UAG suppressor glutamine tRNA(UmUGGIn) in the virus-infected cells. The increased amount of tRNA(UmUGGIn) seems to be important not only for the sufficient production of a viral UAG readthrough protein, but also for the efficient translation of viral mRNAs, since tRNA(UmUGGIn) should read as efficiently the CAA glutamine codon which frequently appears in the viral genome. The increased level of tRNA(UmUGGIn) in virus-infected cells might be due to specific transcription activation of the tRNA gene for tRNA(UmUGGIn). The factor required for the transcription regulation of the suppressor tRNA gene, if it exists in virus infected cells, may not be the same as the factors TFIIIB, IIIC and IIID so far identified. If such a specific transcription factor exists, it would be interesting to characterize it and to elucidate the mechanism by which it is induced by infection with Mo-MuLV or HIV.
Kuchino
Y
Y
Biophysics Division of National Cancer Center Research Institute, Tokyo.
D000241:Adenosine / Q000235:genetics*; D000818:Animals; D000926:Anticodon / Q000235:genetics; D002417:Cattle; D003062:Codon / Q000235:genetics*; D005786:Gene Expression Regulation; D005814:Genes, Viral; D006151:Guanosine / Q000235:genetics*; D006801:Humans; D051379:Mice; D012333:RNA, Messenger / Q000235:genetics*; D012345:RNA, Transfer, Amino Acid-Specific / Q000235:genetics*; D012351:RNA, Transfer, Gln / Q000235:genetics* / Q000378:metabolism; D051381:Rats; D012190:Retroviridae / Q000235:genetics*; D012192:Retroviridae Infections / Q000235:genetics / Q000378:metabolism; D013489:Suppression, Genetic; D014529:Uridine / Q000235:genetics*
D000926:Anticodon; D003062:Codon; D012333:RNA, Messenger; D012345:RNA, Transfer, Amino Acid-Specific; D012351:RNA, Transfer, Gln; D006151:Guanosine; D000241:Adenosine; D014529:Uridine