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Mitochondrial evolution and functions in malaria parasites
Journal article   Peer reviewed

Mitochondrial evolution and functions in malaria parasites

Akhil B Vaidya and Michael W Mather
Annual review of microbiology, v 63(1), pp 249-267
2009
PMID: 19575561

Abstract

Electron Transport Animals Mitochondria - genetics Models, Biological Plasmodium - genetics Plasmodium - physiology Mitochondrial Proteins - genetics Mitochondria - physiology RNA, Ribosomal - genetics Evolution, Molecular
Mitochondria in malaria parasites have some unusual evolutionary and functional features. The drastic reduction in the size of their mitochondrial genome, encoding just three proteins, appears to have originated at the point of divergence of dinoflagellates and apicomplexan parasites from ciliates and may have accompanied the acquisition of plastids by the former. Unusual translational machinery as revealed by the highly fragmented mitochondrial ribosomal RNA genes also appears to have originated at this deflection point. Some of the biochemical properties of malarial mitochondria also appear to be unconventional. Although tricarboxylic acid cycle enzymes are encoded by the genome, they do not appear to be involved in the full oxidation of glucose to fuel mitochondrial ATP synthesis in the blood stages of malaria parasites. A critical role of the mitochondrial electron transport chain appears to be to serve pyrimidine biosynthesis. In spite of their minimal nature, Plasmodium mitochondria are attractive targets for antimalarial drugs.

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Web of Science research areas
Microbiology
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