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Related Concept Videos

Intralumenal Vesicles and Multivesicular Bodies01:38

Intralumenal Vesicles and Multivesicular Bodies

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Intraluminal vesicles (ILVs) are small vesicles 50-80 nm in diameter formed during the maturation of early endosomes. A specialized endosome containing numerous ILVs is called a multivesicular body (MVB). ILVs contain internalized molecules such as antigens, nucleic acids, proteins, and metabolites. Some of these molecules are released from the MVBs inside exosomes and are transported to other cells. Other MVBs contain molecules that are retained in the ILVs and are later degraded within the...
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Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...
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Phosphoinositides and PIPs01:42

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Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
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Membrane Fluidity01:26

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Membrane fluidity is explained by the fluid mosaic model of the cell membrane, which describes the plasma membrane structure as a mosaic of components—including phospholipids, cholesterol, proteins, and carbohydrates—that gives the membrane a fluid character.
Mosaic nature of the membrane
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Vesicular Tubular Clusters01:45

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After budding out from the ER membrane, some COPII vesicles lose their coat and fuse with one another to form larger vesicles and interconnected tubules called vesicular tubular clusters or VTCs. These clusters constitute a compartment at the ER-Golgi interface known as ERGIC (Endoplasmic Reticulum Golgi Intermediate Compartment). The ERGIC is a mobile membrane-bound cargo transport system that sorts proteins secreted from ER and delivers them to the Golgi.
With the help of motor proteins such...
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Receptor-mediated Endocytosis01:20

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Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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MicroRNA-based Regulation of Picornavirus Tropism
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Permeability changes of integrin-containing multivesicular structures triggered by picornavirus entry.

Pan Soonsawad1, Lassi Paavolainen2, Paula Upla2

  • 1Department of Molecular and Cellular Biology, University of California Davis, Davis, California, United States of America; Department of Anatomy, Faculty of Dentistry, Mahidol University, Bangkok, Thailand.

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Picornavirus infection dramatically alters cellular endosomes, forming larger, more complex compartments. These virus-induced multivesicular bodies (MVBs) develop membrane breakages, facilitating viral genome release for replication.

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Area of Science:

  • Cell Biology
  • Virology
  • Structural Biology

Background:

  • Clustered α2β1-integrin uptake forms multivesicular bodies (MVBs).
  • Picornavirus echovirus 1 (EVI) enhances cellular internalization via clustered integrins.
  • Understanding virus-induced endosomal changes is crucial for viral entry mechanisms.

Purpose of the Study:

  • To elucidate the structural and dynamic changes in virus-induced MVBs (vMVBs) during early echovirus 1 infection.
  • To compare vMVBs with antibody-induced control MVBs (mock infection).
  • To investigate the role of vMVB morphology in viral genome release.

Main Methods:

  • High-pressure cryo fixation of infected cells.
  • Immuno electron tomography for 3D structural analysis.
  • Confocal microscopy with neutral-red labeling to assess viral genome release and endosomal permeability.

Main Results:

  • Virus-induced MVBs (vMVBs) showed increased size and complexity of intraluminal vesicles (ILVs) at 2 and 3.5 hours post infection (p.i.) compared to controls.
  • Membrane breakages were observed in vMVBs after 2 and 3.5 h p.i.
  • Virus uncoating initiated by 30 min p.i., with increased vMVB permeability between 1-3 hours p.i.

Conclusions:

  • Echovirus 1 infection induces significant morphological alterations in endosomal compartments.
  • Membrane breakages in vMVBs appear to be a key mechanism for facilitating viral genome release into the cytoplasm.
  • These findings provide insights into the infectious entry pathway of non-enveloped enteroviruses.