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Related Concept Videos

Actin Polymerization and Cell Motility01:13

Actin Polymerization and Cell Motility

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.
Cytoskeletal Coordination in Cell Migration01:32

Cytoskeletal Coordination in Cell Migration

A migrating cell changes its shape during the cyclic events of attachment and detachment from the substratum and repositions the cell organelles correspondingly. These complex events are orchestrated by the dynamic cytoskeletal network comprising actin filaments, intermediate filaments, and microtubules. Cytoskeletal crosstalk — the direct and indirect communication between the different components — is crucial for this coordination. Direct communication involves various linker proteins that...
Formation of Higher-order Actin Filaments01:11

Formation of Higher-order Actin Filaments

The polymerization of G-actin monomers into filamentous F-actin is a multi-step process. Once the F-actins are formed, they can bundle together in different arrangements to form higher-order networks and regulate cellular functions. Common examples include the formation of lamellipodia and filopodia at the cell's leading edge by actin reorganization in a migrating cell. The microvilli on the brush border epithelial cells are also formed through the F-actin network.
The high-order actin networks...
Cell Motility through Blebbing01:16

Cell Motility through Blebbing

Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
Blebbing Through the Matrix
In multicellular...
Mechanism of Lamellipodia Formation01:31

Mechanism of Lamellipodia Formation

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...
Mechanism of Filopodia Formation01:39

Mechanism of Filopodia Formation

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.
Their main function is to guide migrating cells during normal tissue morphogenesis or cancer metastasis by recognizing and making initial contacts with the extracellular matrix. However, they can also act as stationary cell anchors or help to establish communication...

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Related Experiment Video

Updated: May 23, 2026

The Mechanics of (Poro-)Elastic Contractile Actomyosin Networks As a Model System of the Cell Cytoskeleton
08:50

The Mechanics of (Poro-)Elastic Contractile Actomyosin Networks As a Model System of the Cell Cytoskeleton

Published on: March 10, 2023

Coupling actin flow, adhesion, and morphology in a computational cell motility model.

Danying Shao1, Herbert Levine, Wouter-Jan Rappel

  • 1Center for Theoretical Biological Physics and Department of Physics, University of California, San Diego, La Jolla, CA 92093-0374, USA.

Proceedings of the National Academy of Sciences of the United States of America
|April 12, 2012
PubMed
Summary

This study introduces a computational model that explores how cells move by integrating actin flow, adhesion forces, and membrane properties. Using a phase-field method and reaction-diffusion models, the researchers simulate cell motility in fish keratocytes. The model shows that cell velocity and shape depend on actin polymerization, myosin contraction, and adhesion site states. By varying parameters like myosin II activity and adhesion strength, the researchers explore how these factors influence cell behavior. The model successfully reproduces experimental findings on actin flow and stress patterns. It suggests that cell morphology is determined by the balance of multiple forces. The study provides a framework for understanding how physical and biochemical factors interact in cell motility.

Keywords:
actin polymerizationcell migrationadhesion site dynamicscomputational cell biology

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Traction Microscopy Integrated with Microfluidics for Chemotactic Collective Migration
10:53

Traction Microscopy Integrated with Microfluidics for Chemotactic Collective Migration

Published on: October 13, 2019

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Last Updated: May 23, 2026

The Mechanics of (Poro-)Elastic Contractile Actomyosin Networks As a Model System of the Cell Cytoskeleton
08:50

The Mechanics of (Poro-)Elastic Contractile Actomyosin Networks As a Model System of the Cell Cytoskeleton

Published on: March 10, 2023

Traction Microscopy Integrated with Microfluidics for Chemotactic Collective Migration
10:53

Traction Microscopy Integrated with Microfluidics for Chemotactic Collective Migration

Published on: October 13, 2019

Area of Science:

  • Computational cell biology
  • Cell motility mechanisms
  • Biomechanics of cellular processes

Background:

Cell migration remains a complex biological process with multiple interacting components. Prior research has shown that actin polymerization and myosin-driven contraction contribute to cell movement. However, how these forces integrate with adhesion dynamics and membrane properties is not fully understood. No prior work had resolved how discrete adhesion sites influence cell morphology during migration. This paper's contribution lies in combining physical membrane properties with reaction-diffusion models of actin-myosin machinery. The study addresses a gap in understanding how adhesion states affect cell shape and movement. It builds on established knowledge of actin flow patterns in keratocytes but introduces a novel computational framework. The model integrates adhesion site states with actin filament dynamics. This approach allows researchers to explore how varying parameters influence cell behavior. The study's background highlights the need for a unified model of cell motility.

Purpose Of The Study:

The study aims to develop a computational framework that integrates multiple physical and biochemical factors in cell motility. It focuses on how actin flow, adhesion states, and membrane forces interact to determine cell movement. The researchers sought to test this model using fish keratocytes, known for their consistent morphology during migration. They aimed to reproduce experimental findings on actin flow and stress patterns. The study's motivation stems from the lack of a unified model linking adhesion dynamics to cell shape and velocity. The researchers wanted to explore how changing myosin II activity and adhesion strength affects cell behavior. They also aimed to identify how adhesion site states influence actin flow patterns. The purpose is to provide a tool for understanding the physical mechanisms behind cell motility.

Main Methods:

The researchers employed a phase-field method to simulate cell boundary movement with physical membrane properties. They combined this with a reaction-diffusion model for actin-myosin interactions. Discrete adhesion sites were modeled with two states: gripping and slipping. These adhesion sites were integrated with actin filament dynamics modeled as a viscous network. The model was tested using fish keratocytes, known for maintaining morphology during migration. The researchers varied myosin II activity and adhesion strength to explore cell motility phases. They compared model outputs to experimental results on actin flow and stress patterns. The model allowed them to simulate how different parameters affect cell velocity and shape.

Main Results:

The model successfully reproduced experimental findings on actin flow and stress patterns in keratocytes. It showed that cell velocity and morphology depend on actin polymerization, myosin contraction, adhesion forces, and membrane forces. Varying myosin II activity altered actin flow patterns and cell velocity. Increasing adhesion strength changed the cell's shape and movement dynamics. The model demonstrated that adhesion site states influence actin flow distribution. It revealed that the phase diagram of cell motility depends on myosin and adhesion parameters. The simulations matched observed stress patterns in migrating cells. The model suggests that cell morphology is determined by the integration of multiple forces.

Conclusions:

The study concludes that cell motility depends on the integration of actin polymerization, myosin contraction, adhesion forces, and membrane properties. The model suggests that adhesion site states influence actin flow and cell morphology. It supports the idea that cell velocity is determined by the balance of these forces. The findings align with experimental observations of actin flow patterns in keratocytes. The model provides a framework for exploring how varying parameters affect cell behavior. It confirms that myosin II activity and adhesion strength determine motility phases. The study does not propose new drug targets or future research directions. It emphasizes the importance of integrating multiple physical and biochemical factors in cell motility models.

The model suggests that actin flow patterns, myosin contraction, adhesion forces, and membrane forces determine cell morphology and velocity.

Adhesion sites are modeled as discrete units that can switch between gripping and slipping states, influencing actin flow dynamics.

The phase-field method allows for simulating moving cell boundaries with physical membrane properties, essential for modeling cell motility.

Myosin II activity influences cell velocity and actin flow patterns, as shown by the model's phase diagram analysis.

The model successfully reproduces observed actin flow and stress patterns in fish keratocytes, validating its approach.

The findings suggest that cell morphology and movement depend on the integration of multiple physical and biochemical factors.