Functional characterization of mitochondrial translation components in the early diverging eukaryote Toxoplasma gondii.

Mon9  Apr11:45am(15 mins)
Where:
Stream 2 - Llandinam A6
Miss Alice Lacombe

Authors

A Lacombe1; J Tottey1; J Ovciarikova1; L Sheiner1
1 Wellcome Trust Centre for Molecular Parasitology, University of Glasgow, UK

Discussion

Apicomplexan parasites are unicellular eukaryotes. Being early diverging organisms they often possess the universally conserved core of global eukaryotic machineries. Yet, being parasites they often possess unique functions. Studying fundamental mitochondrial biology in these organisms leads to definition of the ancestral core of eukaryotic pathways while simultaneously aiding the identification of new targets for drug development against diseases like malaria. Organelle translation has been a focus for the latter in recent years.

Due to extreme gene transfer to the nuclear genome, the apicomplexan mitochondrial genome encodes only three proteins: COXI, COXIII and COB. Indirect evidence suggests that translation of these proteins in the mitochondrion is active and essential [1], but it is not clear what the ribosome composition is. For example, many of the mitochondrial ribosome 30S subunit components are missing in apicomplexan and it has been proposed that the presence of other proteins, that are not widespread amongst eukaryotes, like S22, S29 and S35, may compensate [2].

Via a new bioinformatics screen [3], we identified candidate components of the apicomplexan mitochondrial translation pathway. Gene tagging and immunofluorescence confirmed the mitochondrial location of 12 out of 15 proteins tested. Conditional knockdown of three of the corresponding genes individually confirmed an expected growth defect upon the depletion of each gene. However, despite growing slowly, Toxoplasma lacking the mitochondrial ribosomal S35 subunit could survive continuously in culture. Moreover, mitochondrial functions like protein import remain unaffected. These surprising findings argue against the current model and raise the question of whether mitochondrial translation is in fact not essential for Toxoplasma.

[1] Pino P, Aeby E, Foth BJ, Sheiner L et al; 2010 Mol Microbiol. 2010 May; 76(3):706-18 [2] Gupta A et al; Open Biol. 2014 May; 4(5): 140045 [3] Sheiner L et al; PLoS Pathog. 2011 Dec; 7(12):e1002392. (49 citations)
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