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  Host Mitochondrial Association Evolved in the Human Parasite Toxoplasma gondii via Neofunctionalization of a Gene Duplicate

Adomako-Ankomah, Y., English, E. D., Danielson, J. J., Pernas, L., Parker, M. L., Boulanger, M. J., et al. (2016). Host Mitochondrial Association Evolved in the Human Parasite Toxoplasma gondii via Neofunctionalization of a Gene Duplicate. Genetics, 203(1), 283-98. doi:10.1534/genetics.115.186270.

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Adomako-Ankomah, Y., Author
English, E. D., Author
Danielson, J. J., Author
Pernas, L.1, Author           
Parker, M. L., Author
Boulanger, M. J., Author
Dubey, J. P., Author
Boyle, J. P., Author
Affiliations:
1Pernas – Metabolism of Infection, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society, ou_3394005              

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Free keywords: Animals Cats Gene Dosage *Gene Duplication Gene Expression Regulation Host-Parasite Interactions/*genetics Mice Mice, Knockout Multigene Family Protozoan Proteins/*genetics Toxoplasma/*genetics Toxoplasmosis/*parasitology Transcription, Genetic *Hammondia hammondi *Neospora caninum *Toxoplasma gondii *neofunctionalization
 Abstract: In Toxoplasma gondii, an intracellular parasite of humans and other animals, host mitochondrial association (HMA) is driven by a gene family that encodes multiple mitochondrial association factor 1 (MAF1) proteins. However, the importance of MAF1 gene duplication in the evolution of HMA is not understood, nor is the impact of HMA on parasite biology. Here we used within- and between-species comparative analysis to determine that the MAF1 locus is duplicated in T. gondii and its nearest extant relative Hammondia hammondi, but not another close relative, Neospora caninum Using cross-species complementation, we determined that the MAF1 locus harbors multiple distinct paralogs that differ in their ability to mediate HMA, and that only T. gondii and H. hammondi harbor HMA(+) paralogs. Additionally, we found that exogenous expression of an HMA(+) paralog in T. gondii strains that do not normally exhibit HMA provides a competitive advantage over their wild-type counterparts during a mouse infection. These data indicate that HMA likely evolved by neofunctionalization of a duplicate MAF1 copy in the common ancestor of T. gondii and H. hammondi, and that the neofunctionalized gene duplicate is selectively advantageous.

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 Dates: 2016-052016
 Publication Status: Issued
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 Identifiers: Other: 26920761
DOI: 10.1534/genetics.115.186270
ISSN: 1943-2631 (Electronic)0016-6731 (Linking)
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Title: Genetics
Source Genre: Journal
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Pages: - Volume / Issue: 203 (1) Sequence Number: - Start / End Page: 283 - 98 Identifier: -