Saturday, May 07, 2016

Dense granule trafficking in Toxoplasma gondii requires a unique class 27 myosin and actin filaments

 2016 May 4. pii: mbc.E15-12-0824. [Epub ahead of print]


Toxoplasma gondii survival within its host cell requires protein release from secretory vesicles, called dense granules (DGs), in order to maintain the parasite's intracellular replicative niche. Despite their importance, nothing is known about the mechanisms underlying DG transport. In higher eukaryotes, secretory vesicles are transported to the plasma membrane by molecular motors moving on their respective cytoskeletal tracks (i.e. microtubules and actin). Since the organization of these cytoskeletal structures differs substantially in Toxoplasma gondii, the molecular motor-dependence of DG trafficking is far from certain. By imaging the motions of GFP-tagged DGs in intracellular parasites with high temporal and spatial resolution, we show through a combination of molecular genetics and chemical perturbations that directed DG transport is independent of microtubules and presumably their kinesin/dynein motors. However, directed DG transport is dependent on filamentous actin and a unique class 27 myosin, TgMyoF, which has structural similarity to myosin V, the prototypical cargo transporter. Acto-myosin DG transport was unexpected since filamentous parasite actin has yet to be visualized in vivo due in part to the prevailing model that parasite actin forms short, unstable filaments. Thus, our data uncover new critical roles for these essential proteins in the lytic cycle of this devastating pathogen.
© 2016 by The American Society for Cell Biology.
[PubMed - as supplied by publisher]

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