Genes mutations identified that allow mitochondrial DNA loss in trypanosomes

In a paper published recently in PNAS, the Schnaufer lab has uncovered the mechanism that allows the disease-causing bloodstream form of the parasite Trypanosoma brucei to survive complete loss of its mitochondrial DNA (mtDNA).

MtDNA loss is the distinguishing feature of a group of trypanosome parasites (so-called dyskinetoplastic trypanosomes), that are transmitted independently of the tsetse fly and are of significant veterinary importance globally.

The work makes the astonishing finding that a single mutation in a nuclear gene, ATP synthase gamma, is fully sufficient to allow wholesale loss of  the mtDNA. The results represent not only a critical advance in our understanding of how these important parasites evolve and how their mitochondrial biology was shaped by host-pathogen relationships, but also have important implications for current efforts to develop much-needed new drugs.

Paper available online in PNAS

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