Haemoglobin S and C affect the motion of Maurer's clefts in Plasmodium falciparum-infected erythrocytes

The haemoglobinopathies S and C protect carriers from severe Plasmodium falciparum malaria. We have recently shown that haemoglobin S and C interfere with host-actin remodelling in parasitized erythrocytes and the generation of an actin network that seems to be required for vesicular protein traffic...

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Main Authors: Kilian, Nicole (Author) , Dittmer, Martin (Author) , Cyrklaff, Marek (Author) , Frischknecht, Friedrich (Author) , Sanchez, Cecilia P. (Author) , Lanzer, Michael (Author)
Format: Article (Journal)
Language:English
Published: 2013
In: Cellular microbiology
Year: 2013, Volume: 15, Issue: 7, Pages: 1111-1126
ISSN:1462-5822
DOI:10.1111/cmi.12102
Online Access:Verlag, Volltext: http://dx.doi.org/10.1111/cmi.12102
Verlag, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1111/cmi.12102
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Author Notes:Nicole Kilian, Martin Dittmer, Marek Cyrklaff, Djeneba Ouermi, Cyrille Bisseye, Jacques Simpore, Friedrich Frischknecht, Cecilia P. Sanchez, Michael Lanzer

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520 |a The haemoglobinopathies S and C protect carriers from severe Plasmodium falciparum malaria. We have recently shown that haemoglobin S and C interfere with host-actin remodelling in parasitized erythrocytes and the generation of an actin network that seems to be required for vesicular protein trafficking from the Maurer's clefts (a parasite-derived intermediary protein secretory organelle) to the erythrocyte surface. Here we show that the actin network exerts skeletal functions by anchoring the Maurer's clefts within the erythrocyte cytoplasm. Using a customized tracking tool to investigate the motion of single Maurer's clefts, we found that a functional actin network restrains Brownian motion of this organelle. Maurer's clefts moved significantly faster in wild-type erythrocytes treated with the actin depolymerizing agent cytochalasin D and in erythrocytes containing the haemoglobin variants S and C. Our data support the model of an impaired actin network being an underpinning cause of cellular malfunctioning in parasitized erythrocytes containing haemoglobin S or C, and, possibly, for the protective role of these haemoglobin variants against severe malaria. 
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