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

2015 ◽  
Vol 43 (4) ◽  
pp. 265-272 ◽  
Author(s):  
Wataru Kagaya ◽  
Shinya Miyazaki ◽  
Kazuhide Yahata ◽  
Nobuo Ohta ◽  
Osamu Kaneko
2021 ◽  
Author(s):  
Olivia M. S. Carmo ◽  
Gerald J Shami ◽  
Dezerae Cox ◽  
Boyin Liu ◽  
Adam J Blanch ◽  
...  

Presentation of the variant antigen, Plasmodium falciparum erythrocyte membrane protein 1 (EMP1), at knob-like protrusions on the surface of infected red blood cells, underpins P. falciparum malaria pathogenicity. Here we describe a protein PF3D7_0301700 (PTP7), that functions at the nexus between the intermediate trafficking organelle, the Maurer’s cleft, and the red blood cell surface. Genetic disruption of PTP7 leads to accumulation of vesicles at the Maurer’s clefts, grossly aberrant knob morphology, and failure to deliver EMP1 to the red blood cell surface.  We show that an expanded low complexity sequence in the C-terminal region of PTP7, found only in the Laverania clade of Plasmodium , is critical for efficient virulence protein trafficking.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Maria del Pilar Quintana ◽  
Jun-Hong Ch’ng ◽  
Kirsten Moll ◽  
Arash Zandian ◽  
Peter Nilsson ◽  
...  

2011 ◽  
Vol 60 (3) ◽  
pp. 313-320 ◽  
Author(s):  
Jean Semé Fils Alexandre ◽  
Kazuhide Yahata ◽  
Satoru Kawai ◽  
Motomi Torii ◽  
Osamu Kaneko

2021 ◽  
Vol 83 ◽  
pp. 102358
Author(s):  
Shinya Miyazaki ◽  
Ben-Yeddy Abel Chitama ◽  
Wataru Kagaya ◽  
Amuza Byaruhanga Lucky ◽  
Xiaotong Zhu ◽  
...  

2008 ◽  
Vol 160 (2) ◽  
pp. 81-89 ◽  
Author(s):  
Laetitia Vincensini ◽  
Gamou Fall ◽  
Laurence Berry ◽  
Thierry Blisnick ◽  
Catherine Braun Breton

2018 ◽  
Vol 9 (5) ◽  
pp. 91-95 ◽  
Author(s):  
Praveen Kumar Vemuri ◽  
Sanjay Madala ◽  
Vijaya Lakshmi Bodiga ◽  
Suryanarayana Veeravalli ◽  
Nithin Chand Kurra

2017 ◽  
Vol 114 (16) ◽  
pp. 4225-4230 ◽  
Author(s):  
Marion Koch ◽  
Katherine E. Wright ◽  
Oliver Otto ◽  
Maik Herbig ◽  
Nichole D. Salinas ◽  
...  

Invasion of the red blood cell (RBC) by the Plasmodium parasite defines the start of malaria disease pathogenesis. To date, experimental investigations into invasion have focused predominantly on the role of parasite adhesins or signaling pathways and the identity of binding receptors on the red cell surface. A potential role for signaling pathways within the erythrocyte, which might alter red cell biophysical properties to facilitate invasion, has largely been ignored. The parasite erythrocyte-binding antigen 175 (EBA175), a protein required for entry in most parasite strains, plays a key role by binding to glycophorin A (GPA) on the red cell surface, although the function of this binding interaction is unknown. Here, using real-time deformability cytometry and flicker spectroscopy to define biophysical properties of the erythrocyte, we show that EBA175 binding to GPA leads to an increase in the cytoskeletal tension of the red cell and a reduction in the bending modulus of the cell’s membrane. We isolate the changes in the cytoskeleton and membrane and show that reduction in the bending modulus is directly correlated with parasite invasion efficiency. These data strongly imply that the malaria parasite primes the erythrocyte surface through its binding antigens, altering the biophysical nature of the target cell and thus reducing a critical energy barrier to invasion. This finding would constitute a major change in our concept of malaria parasite invasion, suggesting it is, in fact, a balance between parasite and host cell physical forces working together to facilitate entry.


2014 ◽  
Vol 12 (2) ◽  
Author(s):  
Zahra Gholami ◽  
Sameereh Hashemi Najafabadi ◽  
Masoud Soleimani

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