Membrane Trafficking Modulation during Entamoeba Encystation
van Aerle, R
van der Giezen, M
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Entamoeba histolytica is an intestinal parasite that infects 50-100 million people and causes up to 55,000 deaths annually. The transmissive form of E. histolytica is the cyst, with a single infected individual passing up to 45 million cysts per day, making cyst production an attractive target for infection control. Lectins and chitin are secreted to form the cyst wall, although little is known about the underlying membrane trafficking processes supporting encystation. As E. histolytica does not readily form cysts in vitro, we assessed membrane trafficking gene expression during encystation in the closely related model Entamoeba invadens. Genes involved in secretion are up-regulated during cyst formation, as are some trans-Golgi network-to-endosome trafficking genes. Furthermore, endocytic and general trafficking genes are up-regulated in the mature cyst, potentially preserved as mRNA in preparation for excystation. Two divergent dynamin-related proteins found in Entamoeba are predominantly expressed during cyst formation. Phylogenetic analyses indicate that they are paralogous to, but quite distinct from, classical dynamins found in human, suggesting that they may be potential drug targets to block encystation. The membrane-trafficking machinery is clearly regulated during encystation, providing an additional facet to understanding this crucial parasitic process.
The authors thank Audrey Farbos, Karen Moore and Konrad Paszkiewicz for facilitating the sequencing experiments. Te Exeter Sequencing Facility was funded by a Wellcome Trust Institutional Strategic Support Award (WT097835MF). MMS acknowledges support from the Iraqi Ministry of Higher Education and Scientifc Research (MOHESR) and the University of Baghdad. MvdG is grateful for support from the University of Exeter and Higher Education Funding Council for England (HEFCE). We thank Marwan Al-Maqtoof and Christian Hacker (both University of Exeter) for technical support. Emily Herman was supported by a Graduate studentship from Alberta Innovates Health Solutions and a Vanier Graduate Scholarship. Work in the Dacks lab is supported by NSERC Discovery Grant (RES0021028). JBD is the Canada Research Chair Tier II in Evolutionary Cell Biology. Te views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.
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Vol. 7, article 12854
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