Vesicle trafficking and membrane remodelling in cytokinesis

2011 ◽  
Vol 437 (1) ◽  
pp. 13-24 ◽  
Author(s):  
Hélia Neto ◽  
Louise L. Collins ◽  
Gwyn W. Gould

All cells complete cell division by the process of cytokinesis. At the end of mitosis, eukaryotic cells accurately mark the site of division between the replicated genetic material and assemble a contractile ring comprised of myosin II, actin filaments and other proteins, which is attached to the plasma membrane. The myosin–actin interaction drives constriction of the contractile ring, forming a cleavage furrow (the so-called ‘purse-string’ model of cytokinesis). After furrowing is completed, the cells remain attached by a thin cytoplasmic bridge, filled with two anti-parallel arrays of microtubules with their plus-ends interdigitating in the midbody region. The cell then assembles the abscission machinery required for cleavage of the intercellular bridge, and so forms two genetically identical daughter cells. We now know much of the molecular detail of cytokinesis, including a list of potential genes/proteins involved, analysis of the function of some of these proteins, and the temporal order of their arrival at the cleavage site. Such studies reveal that membrane trafficking and/or remodelling appears to play crucial roles in both furrowing and abscission. In the present review, we assess studies of vesicular trafficking during cytokinesis, discuss the role of the lipid components of the plasma membrane and endosomes and their role in cytokinesis, and describe some novel molecules implicated in cytokinesis. The present review covers experiments performed mainly on tissue culture cells. We will end by considering how this mechanistic insight may be related to cytokinesis in other systems, and how other forms of cytokinesis may utilize similar aspects of the same machinery.

2018 ◽  
Author(s):  
Charlotte Nugues ◽  
Nordine Helassa ◽  
Dayani Rajamanoharan ◽  
Robert D Burgoyne ◽  
Lee P Haynes

AbstractMitosis, the accurate segregation of duplicated genetic material into what will become two new daughter cells, is accompanied by extensive membrane remodelling and membrane trafficking activities. Early in mitosis, adherent cells partially detach from the substratum, round up and their surface area decreases. This likely results from an endocytic uptake of plasma membrane material. As cells enter cytokinesis they re-adhere, flatten and exhibit an associated increase in surface area. The identity of the membrane donor for this phase of mitosis remains unclear. Here we show by biochemical and imaging approaches that lysosomes undergo exocytosis at telophase and that this requires the activity of phosphatidylinositol 4-kinase-IIIβ. Inhibition of lysosome exocytosis resulted in mitotic failure in a significant proportion of cells suggesting that this facet of lysosome physiology is essential and represents a new regulatory mechanism in mitosis.


2005 ◽  
Vol 33 (6) ◽  
pp. 1290-1294 ◽  
Author(s):  
J. Matheson ◽  
X. Yu ◽  
A.B. Fielding ◽  
G.W. Gould

A crucial facet of mammalian cell division is the separation of two daughter cells by a process known as cytokinesis. An early event in cytokinesis is the formation of an actomyosis contractile ring, which functions like a purse string in the constriction of the forming furrow between the cells. Far less well characterized are the membrane-trafficking steps which deliver new membrane to the cell surface during the plasma membrane expansion known to accompany furrow formation. It is now clearly established that the plasma membrane at the cleavage furrow of mammalian cells has a distinct lipid and protein composition from the rest of the plasma membrane. This may reflect a requirement for both increased surface area during furrowing and for the co-ordinated delivery of intracellular signalling or membrane re-modelling activities to the correct spatial coordinates during cleavage. In this review, we discuss recent work within the area of membrane traffic and cytokinesis.


2010 ◽  
Vol 10 ◽  
pp. 1424-1434 ◽  
Author(s):  
John A. Schiel ◽  
Rytis Prekeris

Cytokinesis is the final stage of mitotic cell division that results in a physical separation of two daughter cells. Cytokinesis begins in the early stages of anaphase after the positioning of the cleavage plane and after the chromosomes segregate. This involves the recruitment and assembly of an actomyosin contractile ring, which constricts the plasma membrane and compacts midzone microtubules to form an electron-dense region, termed the midbody, located within an intracellular bridge. The resolution of this intracellular bridge, known as abscission, is the last step in cytokinesis that separates the two daughter cells. While much research has been done to delineate the mechanisms mediating actomyosin ring formation and contraction, the machinery that is responsible for abscission remains largely unclear. Recent work from several laboratories has demonstrated that dramatic changes occur in cytoskeleton and endosome dynamics, and are a prerequisite for abscission. However, the mechanistic details that regulate the final plasma membrane fusion during abscission are only beginning to emerge and are the subject of considerable controversy. Here we review recent studies within this field and discuss the proposed models of cell abscission.


2021 ◽  
Author(s):  
Govind Kunduri ◽  
Si-Hung Le ◽  
Nagampalli Vijayakrishna ◽  
Daniel Blankenberg ◽  
Izumi Yoshihiro ◽  
...  

AbstractDivision of one cell into two daughter cells is fundamental in all living organisms. Cytokinesis, the final step of cell division, begins with the formation of an actomyosin contractile ring, positioned midway between the segregated chromosomes. Constriction of the ring with concomitant membrane deposition in a spatiotemporal precision generates a cleavage furrow that physically divides the cytoplasm. Unique lipids with specific biophysical properties have been shown to localize to midbodies however, their delivery mechanisms and biological roles were largely unknown. In this study, we show that Ceramide phosphoethanolamine (CPE), the structural analog of sphingomyelin, has unique acyl chain anchors in spermatocytes and is essential for meiosis cytokinesis. We found that disengagement of the central spindle from the contractile ring but not localization of phosphatidyl inositols (PIPs) at the plasma membrane was responsible for the male meiosis cytokinesis defect in CPE deficient animals. Further, we demonstrate that enrichment of CPE in Rab7 and Rab11 positive endosomes which in turn translocate to the cleavage furrows to promote cytokinesis. Our results implicate endosomal delivery of CPE to ingressing membranes is crucial for meiotic cytokinesis.


1978 ◽  
Vol 253 (3) ◽  
pp. 965-973 ◽  
Author(s):  
D. Doyle ◽  
H. Baumann ◽  
B. England ◽  
E. Friedman ◽  
E. Hou ◽  
...  

1960 ◽  
Vol 7 (2) ◽  
pp. 357-366 ◽  
Author(s):  
H. E. Karrer

Diluted India ink was instilled into the nasal cavity of mice and the lungs of some animals were fixed with osmium tetroxide at various intervals after one instillation. The lungs of other animals were fixed after 4, 7, 9, 16, or 18 daily instillations. The India ink was found to be phagocytized almost exclusively by the free alveolar macrophages. A few particles are occasionally seen within thin portions of alveolar epithelium, within the "small" alveolar epithelial cells, or within occasional leukocytes in the lumina of alveoli. The particles are ingested by an invagination process of the plasma membrane resulting in the formation of intracellular vesicles and vacuoles. Ultimately large amounts of India ink accumulate in the cell, occupying substantial portions of the cytoplasm. The surfaces of phagocytizing macrophages show signs of intense motility. Their cytoplasm contains numerous particles, resembling Palade particles, and a large amount of rough surfaced endoplasmic reticulum. These structures are interpreted as indicative of protein synthesis. At the level of resolution achieved in this study the membranes of this reticulum appear as single dense "lines." On the other hand, the plasma membrane and the limiting membranes of vesicles and of vacuoles often exhibit the double-line structure typical of unit membranes (Robertson, 37). The inclusion bodies appear to be the product of phagocytosis. It is believed that some of them derive from the vacuoles mentioned above, and that they correspond to similar structures seen in phase contrast cinemicrographs of culture cells. Their matrix represents phagocytized material. Certain structures within this matrix are considered as secondary and some of these structures possess an ordered form probably indicative of the presence of lipid. The possible origin and the fate of alveolar macrophages are briefly discussed.


2021 ◽  
Vol 22 (15) ◽  
pp. 8165
Author(s):  
Amanda Chantziou ◽  
Kostas Theodorakis ◽  
Hara Polioudaki ◽  
Eelco de Bree ◽  
Marilena Kampa ◽  
...  

In breast cancer, expression of Cluster of Differentiation 24 (CD24), a small GPI-anchored glycoprotein at the cell periphery, is associated with metastasis and immune escape, while its absence is associated with tumor-initiating capacity. Since the mechanism of CD24 sorting is unknown, we investigated the role of glycosylation in the subcellular localization of CD24. Expression and localization of wild type N36- and/or N52-mutated CD24 were analyzed using immunofluorescence in luminal (MCF-7) and basal B (MDA-MB-231 and Hs578T) breast cancer cells lines, as well as HEK293T cells. Endogenous and exogenously expressed wild type and mutated CD24 were found localized at the plasma membrane and the cytoplasm, but not the nucleoplasm. The cell lines showed different kinetics for the sorting of CD24 through the secretory/endocytic pathway. N-glycosylation, especially at N52, and its processing in the Golgi were critical for the sorting and expression of CD24 at the plasma membrane of HEK293T and basal B type cells, but not of MCF-7 cells. In conclusion, our study highlights the contribution of N-glycosylation for the subcellular localization of CD24. Aberrant N-glycosylation at N52 of CD24 could account for the lack of CD24 expression at the cell surface of basal B breast cancer cells.


2011 ◽  
Vol 22 (8) ◽  
pp. 1148-1166 ◽  
Author(s):  
Laura García-Expósito ◽  
Jonathan Barroso-González ◽  
Isabel Puigdomènech ◽  
José-David Machado ◽  
Julià Blanco ◽  
...  

As the initial barrier to viral entry, the plasma membrane along with the membrane trafficking machinery and cytoskeleton are of fundamental importance in the viral cycle. However, little is known about the contribution of plasma membrane dynamics during early human immunodeficiency virus type 1 (HIV-1) infection. Considering that ADP ribosylation factor 6 (Arf6) regulates cellular invasion via several microorganisms by coordinating membrane trafficking, our aim was to study the function of Arf6-mediated membrane dynamics on HIV-1 entry and infection of T lymphocytes. We observed that an alteration of the Arf6–guanosine 5′-diphosphate/guanosine 5′-triphosphate (GTP/GDP) cycle, by GDP-bound or GTP-bound inactive mutants or by specific Arf6 silencing, inhibited HIV-1 envelope–induced membrane fusion, entry, and infection of T lymphocytes and permissive cells, regardless of viral tropism. Furthermore, cell-to-cell HIV-1 transmission of primary human CD4+T lymphocytes was inhibited by Arf6 knockdown. Total internal reflection fluorescence microscopy showed that Arf6 mutants provoked the accumulation of phosphatidylinositol-(4,5)-biphosphate–associated structures on the plasma membrane of permissive cells, without affecting CD4-viral attachment but impeding CD4-dependent HIV-1 entry. Arf6 silencing or its mutants did not affect fusion, entry, and infection of vesicular stomatitis virus G–pseudotyped viruses or ligand-induced CXCR4 or CCR5 endocytosis, both clathrin-dependent processes. Therefore we propose that efficient early HIV-1 infection of CD4+T lymphocytes requires Arf6-coordinated plasma membrane dynamics that promote viral fusion and entry.


Sign in / Sign up

Export Citation Format

Share Document