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

• Verfasst von: Kilian, Nicole [VerfasserIn]
• Verfasst von: Dittmer, Martin [VerfasserIn]
• Verfasst von: Cyrklaff, Marek [VerfasserIn]
• Verfasst von: Frischknecht, Friedrich [VerfasserIn]
• Verfasst von: Sanchez, Cecilia P. [VerfasserIn]
• Verfasst von: Lanzer, Michael [VerfasserIn]
• Titel: Haemoglobin S and C affect the motion of Maurer's clefts in Plasmodium falciparum-infected erythrocytes
• Verf.angabe: Nicole Kilian, Martin Dittmer, Marek Cyrklaff, Djeneba Ouermi, Cyrille Bisseye, Jacques Simpore, Friedrich Frischknecht, Cecilia P. Sanchez, Michael Lanzer
• Jahr: 2013
• Umfang: 16 S.
• Fussnoten: First published online 20 January 2013 ; Gesehen am 23.08.2018
• Titel Quelle: Enthalten in: Cellular microbiology
• Ort Quelle: Oxford [u.a.] : Wiley-Blackwell, 1999
• Jahr Quelle: 2013
• Band/Heft Quelle: 15(2013), 7, Seite 1111-1126
• ISSN Quelle: 1462-5822
• DOI: doi:10.1111/cmi.12102
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1580336965

Abstract

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.