Article

Phagocytosis and Cytokinesis: Do Cells Use Common Tools to Cut and to Eat? Highlights on Common Themes and Differences

CNRS, UMR 8104, Paris, France
Traffic (Impact Factor: 4.35). 01/2013; 14(4). DOI: 10.1111/tra.12045
Source: PubMed

ABSTRACT

Eukaryotic cells with specialized functions often use and adapt common molecular machineries. Recent findings have highlighted that actin polymerization, contractile activity and membrane remodelling with exocytosis of internal compartments are required both for successful phagocytosis, the internalization of particulate material, and for cytokinesis, the last step of cell division. Phagocytosis is induced by the triggering of specific cell surface receptors, which leads to membrane deformation, pseudopod extension and contraction to engulf particles. Cytokinesis relies on intense contractile activity and eventually leads to the physical scission of sister cells. In this review, shared features of signalling, cytoskeletal reorganization and vesicular trafficking used in both phagocytosis and cytokinesis will be described, but we will also highlight non-common mechanisms and questions that remain open in these dynamic areas of research.

    • "They are professional phagocytes that take up pathogens and debris through various opsonic and nonopsonic receptors (e.g., Fc receptors [FcRs] for the Fc portion of immunoglobulins; Flannagan et al., 2012; Canton et al., 2013). Interactions between these receptors and their ligands induce signaling cascades, leading to strong and transient actin polymerization , plasma membrane remodeling, and pseudopod extension around the particulate material (Flannagan et al., 2012; Deschamps et al., 2013; Niedergang, 2016). The closed compartment that forms (the phagosome) loses its actin coat, undergoes fusion and fission with compartments of the endocytic machinery (Botelho and Grinstein, 2011; Fairn and Grinstein, 2012), and eventually fuses with lysosomes. "
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    ABSTRACT: Human immunodeficiency virus type 1 (HIV-1) impairs major functions of macrophages but the molecular basis for this defect remains poorly characterized. Here, we show that macrophages infected with HIV-1 were unable to respond efficiently to phagocytic triggers and to clear bacteria. The maturation of phagosomes, defined by the presence of late endocytic markers, hydrolases, and reactive oxygen species, was perturbed in HIV-1 infected macrophages. We showed that maturation arrest occurred at the level of the EHD3/MICAL-L1 endosomal sorting machinery. Unexpectedly, we found that the regulatory viral protein (Vpr) was crucial to perturb phagosome maturation. Our data reveal that Vpr interacted with EB1, p150(Glued), and dynein heavy chain and was sufficient to critically alter the microtubule plus end localization of EB1 and p150(Glued), hence altering the centripetal movement of phagosomes and their maturation. Thus, we identify Vpr as a modulator of the microtubule-dependent endocytic trafficking in HIV-1 infected macrophages, leading to strong alterations in phagolysosome biogenesis.
    No preview · Article · Oct 2015 · The Journal of Cell Biology
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    • "In all processes Rho-dependent actin polymerization is conducted by formins (Castrillon and Wasserman, 1994; Miklavc et al., 2012; Watanabe et al., 2008), whereas contractility is mediated via ROCK dependent activation of myosin II (Araki et al., 2003; Matsumura et al., 2011; Olazabal et al., 2002; Reichl et al., 2008) and / or cofilin inhibition (Deschamps et al., 2013; Matsui et al., 2002). Considering that bundling, depolymerisation and crosslinking of cytoskeletal filaments has been found in processes as different as cytokinesis, cell migration and phagocytosis (Deschamps et al., 2013) suggest this to be a well conserved and general mechanism for force generation (Sun et al., 2010). "
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    ABSTRACT: In many secretory cells actin and myosin are specifically recruited to the surface of secretory granules following their fusion with the plasma membrane. Actomyosin-dependent compression of fused granules is essential to promote active extrusion of cargo. Yet, little is known about molecular mechanisms regulating actin coat formation and contraction. Here we provide a detailed kinetic analysis of the molecules regulating actin coat contraction on fused lamellar bodies (LBs) in primary alveolar type II cells. We demonstrate that Rock1 and myosin light chain kinase (MLCK) translocate to fused LBs and activate myosin II on actin coats. Yet, myosin II activity is not sufficient for efficient actin coat contraction. In addition, cofilin-1 and α-actinin translocate to actin coats. Rock1-dependent, regulated actin depolymerisation by cofilin-1 in cooperation with actin crosslinking by α-actinin is essential for complete coat contraction. In summary, our data suggest a complementary role for regulated actin depolymerisation/crosslinking and myosin II activity to contract actin coats and drive secretion.
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    • "Post-mitotic cells do not simply break apart. Decades of observations have revealed that cytokinesis proceeds through complex and stereotyped cell shape changes (Barr and Gruneberg, 2007; Deschamps et al., 2013; Eggert et al., 2006; Fededa and Gerlich, 2012; Green et al., 2012; White and Glotzer, 2012), and systematic RNA interference (RNAi)-based screens have revealed that .100 different proteins are directly or indirectly involved in this process in animal cells (Echard et al., 2004; Eggert et al., 2004; Skop et al., 2004). "
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