Actin is required for endocytic trafficking in the malaria parasite Plasmodium falciparum

dc.contributor.authorSmythe, Wynand A
dc.contributor.authorJoiner, Keith A
dc.contributor.authorHoppe, Heinrich C
dc.date.accessioned2016-07-26T10:37:17Z
dc.date.available2016-07-26T10:37:17Z
dc.date.issued2008
dc.date.updated2016-07-12T17:31:46Z
dc.description.abstractThe intra-erythrocytic stages of the malaria parasite endocytose large quantities of the surrounding erythrocyte cytoplasm and deliver it to a digestive food vacuole via endocytic vesicles. Digestion provides amino acids for parasite protein synthesis and is required to maintain the osmotic integrity of the host cell. The parasite endocytic pathway has been described morphologically by electron microscopy, but the molecular mechanisms that mediate and regulate it remain elusive. Given the involvement of actin in endocytosis in other eukaryotes, we have used actin inhibitors to assess the requirement for this protein in the endocytic pathway of the human malaria parasite, Plasmodium falciparum. Treatment of cultures with cytochalasin D did not affect haemoglobin levels in the parasites when co-administered with protease inhibitors, and neither did it affect the uptake of the endocytic tracer horseradish peroxidase, suggesting the absence of actin in the mechanism of endocytosis. However, in the absence of protease inhibitors, treated parasites contained increased levels of haemoglobin due to an accumulation of enlarged endocytic vesicles, as determined by immunofluorescence and electron microscopy, suggesting a role for actin in vesicle trafficking, possibly by mediating vesicle maturation and/or fusion to the digestive vacuole. In contrast to cytochalasin D, treatment with jasplakinolide led to an inhibition of endocytosis, an accumulation of vesicles closer to the plasma membrane and a marked concentration of actin in the parasite cortex. We propose that the stabilization of cortical actin filaments by jasplakinolide interferes with normal endocytic vesicle formation and migration from the cell periphery.en_ZA
dc.identifierhttp://dx.doi.org/10.1111/j.1462-5822.2007.01058.x
dc.identifier.apacitationSmythe, W. A., Joiner, K. A., & Hoppe, H. C. (2008). Actin is required for endocytic trafficking in the malaria parasite Plasmodium falciparum. <i>Cellular Microbiology</i>, http://hdl.handle.net/11427/20757en_ZA
dc.identifier.chicagocitationSmythe, Wynand A, Keith A Joiner, and Heinrich C Hoppe "Actin is required for endocytic trafficking in the malaria parasite Plasmodium falciparum." <i>Cellular Microbiology</i> (2008) http://hdl.handle.net/11427/20757en_ZA
dc.identifier.citationSmythe, W. A., Joiner, K. A., & Hoppe, H. C. (2008). Actin is required for endocytic trafficking in the malaria parasite Plasmodium falciparum. Cellular microbiology, 10(2), 452-464.en_ZA
dc.identifier.issn1462-5814en_ZA
dc.identifier.ris TY - Journal Article AU - Smythe, Wynand A AU - Joiner, Keith A AU - Hoppe, Heinrich C AB - The intra-erythrocytic stages of the malaria parasite endocytose large quantities of the surrounding erythrocyte cytoplasm and deliver it to a digestive food vacuole via endocytic vesicles. Digestion provides amino acids for parasite protein synthesis and is required to maintain the osmotic integrity of the host cell. The parasite endocytic pathway has been described morphologically by electron microscopy, but the molecular mechanisms that mediate and regulate it remain elusive. Given the involvement of actin in endocytosis in other eukaryotes, we have used actin inhibitors to assess the requirement for this protein in the endocytic pathway of the human malaria parasite, Plasmodium falciparum. Treatment of cultures with cytochalasin D did not affect haemoglobin levels in the parasites when co-administered with protease inhibitors, and neither did it affect the uptake of the endocytic tracer horseradish peroxidase, suggesting the absence of actin in the mechanism of endocytosis. However, in the absence of protease inhibitors, treated parasites contained increased levels of haemoglobin due to an accumulation of enlarged endocytic vesicles, as determined by immunofluorescence and electron microscopy, suggesting a role for actin in vesicle trafficking, possibly by mediating vesicle maturation and/or fusion to the digestive vacuole. In contrast to cytochalasin D, treatment with jasplakinolide led to an inhibition of endocytosis, an accumulation of vesicles closer to the plasma membrane and a marked concentration of actin in the parasite cortex. We propose that the stabilization of cortical actin filaments by jasplakinolide interferes with normal endocytic vesicle formation and migration from the cell periphery. DA - 2008 DB - OpenUCT DP - University of Cape Town J1 - Cellular Microbiology LK - https://open.uct.ac.za PB - University of Cape Town PY - 2008 SM - 1462-5814 T1 - Actin is required for endocytic trafficking in the malaria parasite Plasmodium falciparum TI - Actin is required for endocytic trafficking in the malaria parasite Plasmodium falciparum UR - http://hdl.handle.net/11427/20757 ER - en_ZA
dc.identifier.urihttp://hdl.handle.net/11427/20757
dc.identifier.vancouvercitationSmythe WA, Joiner KA, Hoppe HC. Actin is required for endocytic trafficking in the malaria parasite Plasmodium falciparum. Cellular Microbiology. 2008; http://hdl.handle.net/11427/20757.en_ZA
dc.languageengen_ZA
dc.publisherWileyen_ZA
dc.publisher.institutionUniversity of Cape Town
dc.sourceCellular Microbiologyen_ZA
dc.source.urihttp://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1462-5822
dc.titleActin is required for endocytic trafficking in the malaria parasite Plasmodium falciparumen_ZA
dc.typeJournal Articleen_ZA
uct.type.filetypeText
uct.type.filetypeImage
uct.type.publicationResearchen_ZA
uct.type.resourceArticleen_ZA
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