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Membrane Trafficking Modulation during Entamoeba Encystation
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...
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Published in: | Scientific reports 2017-10, Vol.7 (1), p.12854-17, Article 12854 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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. |
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ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/s41598-017-12875-6 |