Permeability of the cell-to-cell membrane channel and its regulation in an insect cell junction

In Vitro ◽  
1980 ◽  
Vol 16 (12) ◽  
pp. 1029-1042 ◽  
Author(s):  
Birgit Rose
Keyword(s):  
Cell Membrane ◽  
Insect Cell ◽  
Cell Junction ◽  
Membrane Channel

scholarly journals α-catenin switches between a slip and a cooperative catch bond with F-actin to regulate cell junction fluidity

2020 ◽  
Author(s):  
C. Arbore ◽  
M Sergides ◽  
L. Gardini ◽  
F.S. Pavone ◽  
M. Capitanio
Keyword(s):  
Cell Membrane ◽  
Actin Cytoskeleton ◽  
Protein Unfolding ◽  
Solid Phase ◽  
Cell Junctions ◽  
Cell Junction ◽  
Laser Tweezers ◽  
Catch Bond ◽  
Membrane Cytoskeleton ◽  
Solid Phase Transition

α-catenin is a crucial protein at cell junctions that provides connection between the actin cytoskeleton and the cell membrane. At adherens junctions (AJs), α-catenin forms heterodimers with β-catenin that are believed to resist force on F-actin. Outside AJs, α-catenin forms homodimers that directly connect the cell membrane to the actin cytoskeleton, but their mechanosensitive properties are inherently unknown. Surprisingly, by using ultra-fast laser tweezers we found that a single α-β-catenin heterodimer does not resist force but instead slips along F-actin in the direction of force. Conversely, the action of 5 to 10 α-β-catenin heterodimers together with unidirectional force applied to F-actin engaged a molecular switch in α-catenin, which unfolded and strongly bound F-actin as a cooperative catch bond. Similarly, an α-catenin homodimer formed an asymmetric catch bond with F-actin triggered by protein unfolding under force. Our data reveal that α-catenin clustering together with intracellular tension engage a fluid-to-solid phase transition at the membrane-cytoskeleton interface.

scholarly journals Differential Incorporation of Cholesterol by Sindbis Virus Grown in Mammalian or Insect Cells

2009 ◽  
Vol 83 (18) ◽  
pp. 9113-9121 ◽  
Author(s):  
Amanda Hafer ◽  
Rebecca Whittlesey ◽  
Dennis T. Brown ◽  
Raquel Hernandez
Keyword(s):  
Cell Membrane ◽  
Cell Lines ◽  
Insect Cell ◽  
Mammalian Cells ◽  
Sindbis Virus ◽  
Insect Cells ◽  
Virus Assembly ◽  
Critical Role ◽  
Insect Cell Line

ABSTRACT Cholesterol has been shown to be essential for the fusion of alphaviruses with artificial membranes (liposomes). Cholesterol has also been implicated as playing an essential and critical role in the processes of entry and egress of alphaviruses in living cells. Paradoxically, insects, the alternate host for alphaviruses, are cholesterol auxotrophs and contain very low levels of this sterol. To further evaluate the role of cholesterol in the life cycle of alphaviruses, the cholesterol levels of the alphavirus Sindbis produced from three different mosquito (Aedes albopictus) cell lines; one other insect cell line, Sf21 from Spodoptera frugiperda; and BHK (mammalian) cells were measured. Sindbis virus was grown in insect cells under normal culture conditions and in cells depleted of cholesterol by growth in serum delipidated by using Cab-O-sil, medium treated with methyl-β-cyclodextrin, or serum-free medium. The levels of cholesterol incorporated into the membranes of the cells and into the virus produced from these cells were determined. Virus produced from these treated and untreated cells was compared to virus grown in BHK cells under standard conditions. The ability of insect cells to produce Sindbis virus after delipidation was found to be highly cell specific and not dependent on the level of cholesterol in the cell membrane. A very low level of cholesterol was required for the generation of wild-type levels of infectious Sindbis virus from delipidated cells. The data show that one role of the virus membrane is structural, providing the stability required for infectivity that may not be provided by the delipidated membranes in some cells. These data show that the amount of cholesterol in the host cell membrane in and of itself has no effect on the process of virus assembly or on the ability of virus to infect cells. Rather, these data suggest that the cholesterol dependence reported for infectivity and assembly of Sindbis virus is a reflection of differences in the insect cell lines used and the methods of delipidation.

scholarly journals The shear stress of it all: the cell membrane and mechanochemical transduction

2007 ◽  
Vol 362 (1484) ◽  
pp. 1459-1467 ◽  
Author(s):  
Charles R White ◽  
John A Frangos
Keyword(s):  
Signal Transduction ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Membrane ◽  
Fluid Shear Stress ◽  
Cell Function ◽  
Vascular Endothelial Cells ◽  
Cell Junction ◽  
Ligand Interaction ◽  
Endothelial Cell Function

As the inner lining of the vessel wall, vascular endothelial cells are poised to act as a signal transduction interface between haemodynamic forces and the underlying vascular smooth-muscle cells. Detailed analyses of fluid mechanics in atherosclerosis-susceptible regions of the vasculature reveal a strong correlation between endothelial cell dysfunction and areas of low mean shear stress and oscillatory flow with flow recirculation. Conversely, steady shear stress stimulates cellular responses that are essential for endothelial cell function and are atheroprotective. The molecular basis of shear-induced mechanochemical signal transduction and the endothelium's ability to discriminate between flow profiles remains largely unclear. Given that fluid shear stress does not involve a traditional receptor/ligand interaction, identification of the molecule(s) responsible for sensing fluid flow and mechanical force discrimination has been difficult. This review will provide an overview of the haemodynamic forces experienced by the vascular endothelium and its role in localizing atherosclerotic lesions within specific regions of the vasculature. Also reviewed are several recent lines of evidence suggesting that both changes in membrane microviscosity linked to heterotrimeric G proteins, and the transmission of tension across the cell membrane to the cell–cell junction where known shear-sensitive proteins are localized, may serve as the primary force-sensing elements of the cell.

scholarly journals THE CELL JUNCTION IN A LAMELLIBRANCH GILL CILIATED EPITHELIUM

1970 ◽  
Vol 47 (2) ◽  
pp. 468-487 ◽  
Author(s):  
P. Satir ◽  
N. B. Gilula
Keyword(s):  
Cell Membrane ◽  
Smooth Endoplasmic Reticulum ◽  
Freshwater Mussel ◽  
Septate Junction ◽  
Cell Junction ◽  
Junctional Complex ◽  
Regional Differentiation ◽  
Ion Permeability ◽  
Membrane Surfaces ◽  
Entire Cell

The junctional complex in the gill epithelium of the freshwater mussel (Elliptio complanatus) consists of an intermediary junction followed by a 2–3 µ long septate junction. Homologous and heterologous cell pairs are connected by this junction. After fixation with 1% OsO4 containing 1% potassium pyroantimonate, electron microscopy of the gill reveals deposits of electron-opaque precipitate, specifically and consistently localized along cellular membranes. In both junctional and nonjunctional membrane regions, the precipitate usefully outlines the convolutions without obliterating the 150 A intercellular space, which suggests the rarity or absence of either vertebrate-type gap or tight junctions along the entire cell border. The precipitate appears on the cytoplasmic side of the limiting unit membranes of frontal (F), laterofrontal (LF), intermediate (I), lateral (L), and postlateral (PL) cells. The membrane surfaces of certain vesicles of the smooth endoplasmic reticulum, of multivesicular bodies, and of mitochondrial cristae contain precipitate, as does the nucleolus. In other portions of the cell, precipitate is largely absent. The amount of over-all deposition is variable and depends on the treatment of the tissue prior to fixation. Deposition is usually enhanced by pretreatment with 40 mM NaCl as opposed to 40 mM KCl, which suggests that the precipitate is in part sodium pyroantimonate. Treatment with 0.2 mM ouabain does not enhance deposition. Regional differentiation of cell membranes with respect to their ability to precipitate pyroantimonate is found in at least three instances: (a) between the ciliary membranes and other portions of the cell membrane: the precipitate terminates abruptly at the ciliary base, (b) between the LF and I cell borders: the precipitate is asymmetric, favoring the LF side of the junction, and (c) between the septate junctional membrane and adjacent membrane: the precipitate occurs periodically throughout the septate junction region with the periodicity corresponding to the spacing of the septa. This suggests that different regions of the cell membrane may have differing ion permeability properties and, in particular, that the septa may be the regions of high ion permeability in the septate junction.

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