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

Cell Microbiol. 2013 Jul;15(7):1111-26. doi: 10.1111/cmi.12102. Epub 2013 Jan 20.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Erythrocytes / metabolism*
  • Erythrocytes / parasitology*
  • Hemoglobin C / metabolism*
  • Hemoglobin, Sickle / metabolism*
  • Host-Pathogen Interactions
  • Organelles / metabolism*
  • Organelles / parasitology*
  • Plasmodium falciparum / metabolism*


  • Actins
  • Hemoglobin, Sickle
  • Hemoglobin C