Maurer’s Clefts | ScienceGate

In this study, we investigated stage specific expression, trafficking, solubility and topology of endogenous PfMC-2TM in P. falciparum (3D7) infected erythrocytes. Following Brefeldin A (BFA) treatment of parasites, PfMC-2TM traffic was evaluated using immunofluorescence with antibodies reactive with PfMC-2TM. PfMC-2TM is sensitive to BFA treatment and permeabilization of infected erythrocytes with streptolysin O (SLO) and saponin, showed that the N and C-termini of PfMC-2TM are exposed to the erythrocyte cytoplasm with the central portion of the protein protected in the MC membranes. PfMC-2TM was expressed as early as 4 h post invasion (hpi), was tightly colocalized with REX-1 and trafficked to the erythrocyte membrane without a change in solubility. PfMC-2TM associated with the MC and infected erythrocyte membrane and was resistant to extraction with alkaline sodium carbonate, suggestive of protein-lipid interactions with membranes of the MC and erythrocyte. PfMC-2TM is an additional marker of the nascent MCs.

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The Cytoplasmic Region of Plasmodium falciparum SURFIN4.2 Is Required for Transport from Maurer’s Clefts to the Red Blood Cell Surface

Tropical Medicine and Health ◽

10.2149/tmh.2015-38 ◽

2015 ◽

Vol 43 (4) ◽

pp. 265-272 ◽

Cited By ~ 5

Author(s):

Wataru Kagaya ◽

Shinya Miyazaki ◽

Kazuhide Yahata ◽

Nobuo Ohta ◽

Osamu Kaneko

Keyword(s):

Plasmodium Falciparum ◽

Cell Surface ◽

Blood Cell ◽

Red Blood Cell ◽

Cytoplasmic Region ◽

Maurer's Clefts

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A novel Plasmodium falciparum ring stage protein, REX, is located in Maurer’s clefts

Molecular and Biochemical Parasitology ◽

10.1016/j.molbiopara.2004.03.013 ◽

2004 ◽

Vol 136 (2) ◽

pp. 181-189 ◽

Cited By ~ 73

Author(s):

Paula L. Hawthorne ◽

Katharine R. Trenholme ◽

Tina S. Skinner-Adams ◽

Tobias Spielmann ◽

Katja Fischer ◽

...

Keyword(s):

Plasmodium Falciparum ◽

Ring Stage ◽

Maurer's Clefts

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Proteomic Analysis Identifies Novel Proteins of the Maurer’s Clefts, a Secretory Compartment DeliveringPlasmodium falciparumProteins to the Surface of Its Host Cell

Molecular & Cellular Proteomics ◽

10.1074/mcp.m400176-mcp200 ◽

2005 ◽

Vol 4 (4) ◽

pp. 582-593 ◽

Cited By ~ 92

Author(s):

Laetitia Vincensini ◽

Sophie Richert ◽

Thierry Blisnick ◽

Alain Van Dorsselaer ◽

Emmanuelle Leize-Wagner ◽

...

Keyword(s):

Host Cell ◽

Proteomic Analysis ◽

Novel Proteins ◽

Maurer's Clefts

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Maurer’s clefts—a novel secretory organelle?

Molecular and Biochemical Parasitology ◽

10.1016/s0166-6851(03)00212-3 ◽

2003 ◽

Vol 132 (1) ◽

pp. 17-26 ◽

Cited By ~ 49

Author(s):

Jude M. Przyborski ◽

Hannes Wickert ◽

Georg Krohne ◽

Michael Lanzer

Keyword(s):

Maurer's Clefts

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Plasmodium falciparum STEVOR Proteins Are Highly Expressed in Patient Isolates and Located in the Surface Membranes of Infected Red Blood Cells and the Apical Tips of Merozoites

Infection and Immunity ◽

10.1128/iai.01460-07 ◽

2008 ◽

Vol 76 (7) ◽

pp. 3329-3336 ◽

Cited By ~ 51

Author(s):

Jane E. Blythe ◽

Xue Yan Yam ◽

Claudia Kuss ◽

Zbynek Bozdech ◽

Anthony A. Holder ◽

...

Keyword(s):

Plasmodium Falciparum ◽

Multigene Family ◽

Blood Cells ◽

Antigenic Variation ◽

Human Parasite ◽

Host Parasite Interactions ◽

Maurer's Clefts ◽

Host Parasite ◽

Family Code

ABSTRACT The human parasite Plasmodium falciparum has the potential to express a vast repertoire of variant proteins on the surface of the infected red blood cell (iRBC). Variation in the expression pattern of these proteins is linked to antigenic variation and thereby evasion of host antibody-mediated immunity. The genes in the stevor multigene family code for small variant antigens that are expressed in blood-stage parasites where they can be detected in membranous structures called Maurer's clefts (MC). Some studies have indicated that STEVOR protein may also be trafficked to the iRBC membrane. To address the location of STEVOR protein in more detail, we have analyzed expression in several cultured parasite lines and in parasites obtained directly from patients. We detected STEVOR expression in a higher proportion of parasites recently isolated from patients than in cultured parasite lines and show that STEVOR is trafficked in schizont-stage parasites from the MC to the RBC cytosol and the iRBC membrane. Furthermore, STEVOR protein is also detected at the apical end of merozoites. Importantly, we show that culture-adapted parasites do not require STEVOR for survival. These findings provide new insights into the role of the stevor multigene family during both the schizont and merozoite stages of the parasite and highlight the importance of studying freshly isolated parasites, rather than parasite lines maintained in culture, when investigating potential mediators of host-parasite interactions.

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