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Nucleic Acids Research, 2000, Vol. 28, No. 10 2043-2048
© 2000 Oxford University Press

Repair of tRNAs in metazoan mitochondria

Andreas S. Reichert and Mario Mörl*

Max-Planck-Institute for Evolutionary Anthropology, Inselstraße 22, 04103 Leipzig, Germany

The integrity of 3'-ends of tRNAs is essential for aminoacylation and consequently for protein synthesis. The CCA-termini are generated and, if truncated by exonucleolytic activity, restored by tRNA nucleotidyltransferase. However, further truncations at the 3'-end can occur by exonuclease activity or during processing of overlapping tRNA primary transcripts in metazoan mitochondria. In the latter case, the upstream tRNA is released in a 3'-truncated form (lacking up to six bases) and subsequently completed. In human mitochondria, tRNATyr (missing the discriminator nucleotide A73) is completed by a discriminator adding activity followed by CCA addition. Since in vivo a high percentage of further 3'-terminally degraded human tRNATyr transcripts could be observed, it was tested in an in vitro system whether this repair mechanism for tRNA 3'-ends acts also on these further degraded tRNA versions. Additionally, 3'-truncated versions of two non-overlapping mitochondrial tRNAs (tRNAThr and tRNAPhe) were examined. The results show that these transcripts can be repaired during incubation. A similar base incorporating activity was observed in mouse mitochondria, indicating that a repair mechanism for the 3'-end of several tRNAs exists in mitochondria of humans and possibly other metazoans which goes beyond the CCA addition.

* To whom correspondence should be addressed. Tel: +49 341 99 52 507; Fax: +49 341 99 52 555; Email: moerl@eva.mpg.de


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