Publications by authors named "Ronald Drew Etheridge"

Article Synopsis
  • Trypanosoma cruzi, a parasite reliant on heme, regulates its heme levels by adjusting the expression of a specific protein called TcHRG when exposed to free heme in culture.
  • The study found that TcHRG responds similarly to both bound (hemoglobin) and free heme, located near the flagellar pocket and mitochondria.
  • Interestingly, despite the absence of endocytosis, parasites can still acquire heme from hemoglobin, suggesting that TcHRG plays a key role in breaking down hemoglobin to extract heme from outside the cell through the flagellar pocket.
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is a zoonotic protist pathogen that infects up to one third of the human population. This apicomplexan parasite contains three genome sequences: nuclear (65 Mb); plastid organellar, ptDNA (35 kb); and mitochondrial organellar, mtDNA (5.9 kb of non-repetitive sequence).

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is a zoonotic protist pathogen that infects up to 1/3 of the human population. This apicomplexan parasite contains three genome sequences: nuclear (63 Mb); plastid organellar, ptDNA (35 kb); and mitochondrial organellar, mtDNA (5.9 kb of non-repetitive sequence).

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, a heme auxotrophic parasite, can control intracellular heme content by modulating HRG expression when a free heme source is added to axenic culture. Herein, we explore the role of HRG protein in regulating the uptake of heme derived from hemoglobin in epimastigotes. It was found that the parasités endogenous HRG (protein and mRNA) responds similarly to bound (hemoglobin) and free (hemin) heme.

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Eating is fundamental and from this basic principle, living organisms have evolved innumerable strategies to capture energy and nutrients from their environment. As part of the world's aquatic ecosystems, the expansive family of heterotrophic protozoans uses self-generated currents to funnel prokaryotic prey into an ancient, yet highly enigmatic, oral apparatus known as the cytostome-cytopharynx complex prior to digestion. Despite its near ubiquitous presence in protozoans, little is known mechanistically about how this feeding organelle functions.

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Of the pathogenic trypanosomatids, alone retains an ancient feeding apparatus known as the cytotome-cytoharynx omplex (SPC) that it uses as its primary mode of endocytosis in a manner akin to its free-living kinetoplastid relatives who capture and eat bacterial prey via this endocytic organelle. In a recent report, we began the process of dissecting how this organelle functions by identifying the first SPC-specific proteins in Here, we continued these studies and report on the identification of the first enzymatic component of the SPC, a previously identified orphan myosin motor (MyoF) specifically targeted to the SPC. We overexpressed MyoF as a dominant-negative mutant, resulting in parasites that, although viable, were completely deficient in measurable endocytosis To our surprise, however, a full deletion of MyoF demonstrated only a decrease in the overall rate of endocytosis, potentially indicative of redundant myosin motors at work.

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The etiological agent of Chagas disease, , is an obligate intracellular parasite that infects an estimated 7 million people in the Americas, with an at-risk population of 70 million. Despite its recognition as the highest impact parasitic infection of the Americas, Chagas disease continues to receive insufficient attention and resources in order to be effectively combatted. Unlike the other parasitic trypanosomatids that infect humans ( and spp.

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