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Related Concept Videos

Actin Polymerization and Cell Motility01:13

Actin Polymerization and Cell Motility

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Actin is a family of globular proteins that are highly abundant in eukaryotic cells. It makes up approximately 1-5% of total cell protein concentration. Actin monomers polymerize to form a complex network of polarized filaments, the actin cytoskeleton, that plays a crucial role in many cellular processes, including cell motility, division, endocytosis, and metastasis of cancer cells.
Actin cytoskeleton dynamics can produce pushing, pulling, and resistance forces that help the cell to migrate....
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Mechanism of Lamellipodia Formation01:31

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Cells migrating in response to external stimuli form lamellipodia, which are thin membrane protrusions supported by a mesh of linked, branched, or unbranched actin filaments. These actin filaments interact with myosin motor proteins, creating the dynamic actomyosin complex within the cytoskeleton. Contractility, or the ability to generate contractile stress, is inherent to the actomyosin complex. It helps cells detect the stiffness of the surrounding ECM and exert contractile force for...
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Mechanism of Filopodia Formation01:39

Mechanism of Filopodia Formation

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Filopodia are thin, actin-rich cellular protrusions that play an important role in many fundamental cellular functions. They vary in their occurrence, length, and positioning in different cell types, suggesting their diverse roles.
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Actin Filament Depolymerization01:19

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Actin filaments (F-actin) are composed of actin subunits. The dissociation of actin monomers can occur from either end of F-actin. The rate of dissociation is faster from the minus-end or the pointed end, where the actin subunits exist with a bound ADP, together known as ADP-actin. The depolymerization of F-actin is aided by proteins, including the actin-depolymerizing factor (ADF) and cofilin family of proteins, gelsolin, and glia maturation factor (GMF).
In F-actin, the ADF/cofilin proteins...
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Generation of Straight or Branched Actin Filaments01:14

Generation of Straight or Branched Actin Filaments

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The straight or branched structure formation of actin filaments is controlled by nucleating proteins such as the formins and Arp2/3 complex. Formin-mediated assembly results in straight filaments, whereas Arp2/3 protein complex-mediated assembly results in branched actin filaments.
Arp2/3 Complex
Arp2/3 complex is a seven-subunit complex consisting of two proteins similar to actin- Arp2 and Arp3, and five other subunits that help keep Arp2 and Arp3 inactive. When required, the complex is...
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Intracellular Movement of Viruses and Bacteria01:10

Intracellular Movement of Viruses and Bacteria

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Intracellular bacteria and viruses often comprise a group of highly infectious pathogens that can cause several diseases. Bacterial pathogens include those belonging to the genus Rickettsia responsible for conditions such as rocky mountain spotted fever and the Mediterranean spotted fever; Chlamydia, a genus responsible for a sexually transmitted disease; Coxiella burnetii, an agent responsible for Q fever. Viral pathogens include vaccinia—a poxvirus, and herpes simplex virus—a...
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Updated: Jun 7, 2025

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
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WAVE1 and WAVE2 facilitate human papillomavirus-driven actin polymerization during cellular entry.

D J Fernandez1, Stephanie Cheng1, Ruben Prins1

  • 1Department of Molecular Microbiology & Immunology and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, United States.

Biorxiv : the Preprint Server for Biology
|November 18, 2024
PubMed
Summary

Wiskott-Aldrich syndrome proteins WAVE1 and WAVE2 are essential for Human Papillomavirus Type 16 (HPV16) infection. These proteins mediate actin reorganization, facilitating HPV16 entry into epithelial cells via filopodia formation.

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Area of Science:

  • Cell Biology
  • Virology
  • Molecular Biology

Background:

  • Human Papillomavirus Type 16 (HPV16) causes human cancers and requires endocytosis for infection.
  • The precise mechanism by which HPV16 triggers actin reorganization for cell entry remains unclear.

Purpose of the Study:

  • To investigate the role of Wiskott-Aldrich syndrome protein family verprolin-homologous proteins 1 and 2 (WAVE1 and WAVE2) in HPV16 endocytosis.
  • To elucidate how HPV16-cell surface interactions initiate actin-driven endocytosis.

Main Methods:

  • Post-transcriptional gene silencing and genome editing to assess WAVE1 and WAVE2 function.
  • Confocal fluorescence microscopy to analyze colocalization of HPV16, WAVE1, WAVE2, and actin.
  • Quantification of HPV16 internalization rates in cells with modified WAVE protein levels.

Main Results:

  • WAVE1 and WAVE2 are critical for efficient HPV16 infection; their absence significantly reduces HPV16 internalization.
  • Restoration of WAVE1 or WAVE2 in knockout cells rescues HPV16 infection.
  • HPV16, WAVE1, WAVE2, and actin colocalize at the cellular dorsal surface, with HPV16 stimulating filopodia formation mediated by WAVE1 and WAVE2.

Conclusions:

  • WAVE1 and WAVE2 are key molecular mediators of actin polymerization required for HPV16 endocytosis.
  • HPV16 infection is controlled by actin reorganization into filopodial protrusions, a process mediated by WAVE1 and WAVE2.