Rab11A-Controlled Assembly of the Inner Membrane Complex Is Required for Completion of Apicomplexan Cytokinesis

PLoS Pathogens

Manuel Rauch¹  Markus Meissner¹  Angelika Kretzschmar¹  Carolina Agop-Nersesian¹  Gordon Langsley²  Bernina Naissant²  Fathia Ben Rached²  David J. P. Ferguson³  Sabine Thiberge⁴  Robert Menard⁴ 

[1] Hygieneinstitut, Department of Parasitology, University Hospital Heidelberg, Heidelberg, Germany;Laboratoire de Biologie Cellulaire Comparative des Apicomplexes, Department of Infectious Diseases, Institut Cochin, Inserm U567, CNRS UMR 8104, Faculté de Médecine Paris V – Hôpital Cochin, Paris, France;Nuffield Department of Pathology, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom;Unité de Biologie et Génétique du Paludisme, Institut Pasteur, Paris, France

关键词: Parasite replication;    Plasmodium;    Cell cycle;    cell division;    Cell membranes;    Toxoplasma gondii;    Myosins;    Apicomplexa;    Cellular structures;    organelles;   

DOI  :  10.1371/journal.ppat.1000270

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

The final step during cell division is the separation of daughter cells, a process that requires the coordinated delivery and assembly of new membrane to the cleavage furrow. While most eukaryotic cells replicate by binary fission, replication of apicomplexan parasites involves the assembly of daughters (merozoites/tachyzoites) within the mother cell, using the so-called Inner Membrane Complex (IMC) as a scaffold. After de novo synthesis of the IMC and biogenesis or segregation of new organelles, daughters bud out of the mother cell to invade new host cells. Here, we demonstrate that the final step in parasite cell division involves delivery of new plasma membrane to the daughter cells, in a process requiring functional Rab11A. Importantly, Rab11A can be found in association with Myosin-Tail-Interacting-Protein (MTIP), also known as Myosin Light Chain 1 (MLC1), a member of a 4-protein motor complex called the glideosome that is known to be crucial for parasite invasion of host cells. Ablation of Rab11A function results in daughter parasites having an incompletely formed IMC that leads to a block at a late stage of cell division. A similar defect is observed upon inducible expression of a myosin A tail-only mutant. We propose a model where Rab11A-mediated vesicular traffic driven by an MTIP-Myosin motor is necessary for IMC maturation and to deliver new plasma membrane to daughter cells in order to complete cell division.

【 授权许可】

CC BY