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Nucleic Acids Research Advance Access originally published online on March 16, 2008
Nucleic Acids Research 2008 36(8):2654-2666; doi:10.1093/nar/gkn112
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Nucleic Acids Research, 2008, Vol. 36, No. 8 2654-2666
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

RNA

The bacterial and mitochondrial ribosomal A-site molecular switches possess different conformational substates

Jiro Kondo and Eric Westhof*

Architecture et Réactivité de l’ARN, Université Louis Pasteur, Institut de Biologie Moléculaire et Cellulaire, CNRS, 15 rue René Descartes, 67084 Strasbourg, France

*To whom correspondence should be addressed. Tel: +33 3 88 41 70 46; Fax: +33 3 88 60 18 22; Email: E.Westhof{at}ibmc.u-strasbg.fr

Received January 5, 2008. Revised February 9, 2008. Accepted February 18, 2008.

The A site of the small ribosomal subunit participates in the fidelity of decoding by switching between two states, a resting ‘off’ state and an active decoding ‘on’ state. Eight crystal structures of RNA duplexes containing two minimal decoding A sites of the Homo sapiens mitochondrial wild-type, the A1555G mutant or bacteria have been solved. The resting ‘off’ state of the mitochondrial wild-type A site is surprisingly different from that of the bacterial A site. The mitochondrial A1555G mutant has two types of the ‘off’ states; one is similar to the mitochondrial wild-type ‘off’ state and the other is similar to the bacterial ‘off’ state. Our present results indicate that the dynamics of the A site in bacteria and mitochondria are different, a property probably related to the small number of tRNAs used for decoding in mitochondria. Based on these structures, we propose a hypothesis for the molecular mechanism of non-syndromic hearing loss due to the mitochondrial A1555G mutation.


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