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Nucleic Acids Research 2005 33(11):3606-3613; doi:10.1093/nar/gki677
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Published online 22 June 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oupjournals.org

Article

A T-stem slip in human mitochondrial tRNALeu(CUN) governs its charging capacity

Rui Hao1, Ming-Wei Zhao1, Zhan-Xi Hao1, Yong-Neng Yao and En-Duo Wang1,*

State Key Laboratory of Molecular Biology, Shanghai Institutes for Biological Sciences, The Chinese Academy of Sciences 320 Yue Yang Road, Shanghai 200031, People's Republic of China 1Graduate School of the Chinese Academy of Sciences, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, The Chinese Academy of Sciences 320 Yue Yang Road, Shanghai 200031, People's Republic of China

*To whom correspondence should be addressed. Tel: +86 21 54921241; Fax: +86 21 54921011; Email: edwang{at}sibs.ac.cn

Received April 7, 2005. Revised June 9, 2005. Accepted June 9, 2005.

The human mitochondrial tRNALeu(CUN) [hmtRNALeu(CUN)] corresponds to the most abundant codon for leucine in human mitochondrial protein genes. Here, in vitro studies reveal that the U48C substitution in hmtRNALeu(CUN), which corresponds to the pathological T12311C gene mutation, improved the aminoacylation efficiency of hmtRNALeu(CUN). Enzymatic probing suggested a more flexible secondary structure in the wild-type hmtRNALeu(CUN) transcript compared with the U48C mutant. Structural analysis revealed that the flexibility of hmtRNALeu(CUN) facilitates a T-stem slip resulting in two potential tertiary structures. Several rationally designed tRNALeu(CUN) mutants were generated to examine the structural and functional consequences of the T-stem slip. Examination of these hmtRNALeu(CUN) mutants indicated that the T-stem slip governs tRNA accepting activity. These results suggest a novel, self-regulation mechanism of tRNA structure and function.


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