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Nucleic Acids Research 2006 34(8):2472-2481; doi:10.1093/nar/gkl327
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Published online 9 May 2006

© The Author 2006. 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@oxfordjournals.org

Article

Complete DNA sequences of the mitochondrial genomes of the pathogenic yeasts Candida orthopsilosis and Candida metapsilosis: insight into the evolution of linear DNA genomes from mitochondrial telomere mutants

Peter Kosa1, Matus Valach1, Lubomir Tomaska2, Kenneth H. Wolfe3 and Jozef Nosek1,*

1 Department of Biochemistry, Faculty of Natural Sciences, Comenius University Mlynska dolina CH-1 and B-1, 842 15, Bratislava, Slovak Republic 2 Department of Genetics, Faculty of Natural Sciences, Comenius University Mlynska dolina CH-1 and B-1, 842 15, Bratislava, Slovak Republic 3 Smurfit Institute of Genetics, University of Dublin, Trinity College Dublin 2, Ireland

*To whom correspondence should be addressed. Tel: +421 2 60296 536; Fax: +421 2 60296 452; Email: nosek{at}fns.uniba.sk

Received January 13, 2006. Revised February 7, 2006. Accepted April 13, 2006.

We determined complete mitochondrial DNA sequences of the two yeast species, Candida orthopsilosis and Candida metapsilosis, and compared them with the linear mitochondrial genome of their close relative, C.parapsilosis. Mitochondria of all the three species harbor compact genomes encoding the same set of genes arranged in the identical order. Differences in the length of these genomes result mainly from the presence/absence of introns. Multiple alterations were identified also in the sequences of the ribosomal and transfer RNAs, and proteins. However, the most striking feature of C.orthopsilosis and C.metapsilosis is the existence of strains differing in the molecular form of the mitochondrial genome (circular-mapping versus linear). Their analysis opens a unique window for understanding the role of mitochondrial telomeres in the stability and evolution of molecular architecture of the genome. Our results indicate that the circular-mapping mitochondrial genome derived from the linear form by intramolecular end-to-end fusions. Moreover, we suggest that the linear mitochondrial genome evolved from a circular-mapping form present in a common ancestor of the three species and, at the same time, the emergence of mitochondrial telomeres enabled the formation of linear monomeric DNA forms. In addition, comparison of isogenic C.metapsilosis strains differing in the form of the organellar genome suggests a possibility that, under some circumstances, the linearity and/or the presence of telomeres provide a competitive advantage over a circular-mapping mitochondrial genome.


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