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Mitochondrial genome diversity: evolution of the molecular architecture and replication strategy

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Abstract

Mitochondrial genomes in organisms from diverse phylogenetic groups vary in both size and molecular form. Although the types of mitochondrial genome appear very dissimilar, several lines of evidence argue that they do not differ radically. This would imply that interconversion between different types of mitochondrial genome might have occurred via relatively simple mechanisms. We exemplify this scenario on patterns accompanying evolution of mitochondrial telomeres. We propose that mitochondrial telomeres are derived from mobile elements (transposons or plasmids) that invaded mitochondria, integrated into circular or polydisperse linear mitochondrial DNAs (mtDNAs) and subsequently enabled precise resolution of the linear genophore. Simply, the selfish elements generated a problem — how to maintain the ends of a linear DNA — and, at the same time, made themselves essential by providing its solution. This scenario implies that insertion or deletion of such resolution elements may represent relatively simple routes for interconversion between different forms of the mitochondrial genome.

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Acknowledgements

We thank L. Kováč (Comenius University, Bratislava, Slovakia) and H. Fukuhara (Institut Curie, Orsay, France) for continuous support, helpful discussions and comments. M. Kucej, B. Kucejova (Comenius University, Bratislava, Slovakia), T. Cesare, D. Subramanian, (University of North Carolina, Chapel Hill, N.C., USA) and R. Resnick (Cornell University, Ithaca, N.Y., USA) are acknowledged for valuable editorial advice. The work in our laboratory is supported by grants from the Howard Hughes Medical Institute (55000327), the Slovak grant agencies VEGA (1/9153/02 and 1/0006/03) and APVT (20-003902), and the Fogarty International Research Collaboration Award (1-R03-TW05654-01). J.N. was supported by an EMBO short term fellowship.

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Nosek, J., Tomáška, Ľ. Mitochondrial genome diversity: evolution of the molecular architecture and replication strategy. Curr Genet 44, 73–84 (2003). https://doi.org/10.1007/s00294-003-0426-z

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