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Related Concept Videos

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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
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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.
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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...
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Polymerization force-regulated actin filament-Arp2/3 complex interaction dominates self-adaptive cell migrations.

Xindong Chen1,2, Yuhui Li3, Ming Guo4

  • 1Institute of Biomechanics and Medical Engineering, Department of Engineering Mechanics, Tsinghua University, Beijing 100084, China.

Proceedings of the National Academy of Sciences of the United States of America
|August 28, 2023
PubMed
Summary

Cells adapt their movement to complex environments using a novel "resistance-adaptive propulsion" theory. This model explains how protein interactions enable cells to navigate obstacles and utilize resources efficiently during migration.

Keywords:
Arp2/3 complexbranched actin filamentspropulsive forceself-adaptive cell migrations

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Area of Science:

  • Cell Biology
  • Biophysics
  • Computational Biology

Background:

  • Cell migration is crucial for cancer invasion and immune responses.
  • Understanding the molecular mechanisms driving cell adaptation to heterogeneous microenvironments is limited.
  • Experimental probing of millisecond-scale protein dynamics in cell migration is challenging.

Purpose of the Study:

  • To establish a theory and multiscale modeling system explaining how cells adapt migration to complex extracellular microenvironments (ECMs).
  • To elucidate the molecular interactions governing self-adaptive cell propulsion and morphological changes.

Main Methods:

  • Developed a spatiotemporal
  • resistance-adaptive propulsion
  • theory.
  • Created a multiscale dynamic modeling system from protein interactions to whole-cell behavior.
  • Analyzed the roles of Arp2/3 complexes and actin filament dynamics.

Main Results:

  • Cells self-adapt propulsive forces to heterogeneous ECMs via resistance-triggered positive and negative feedback mechanisms.
  • Positive feedback, driven by actin filament bending and Arp2/3 binding, enhances propulsion.
  • Negative feedback hinders branched filament assembly in high-resistance areas, enabling obstacle circumvention.
  • Cell migration velocity exhibits temporal hysteresis due to cytoskeleton remodeling.
  • Directional migration depends on ECM stiffness and local actin polymerization rates.

Conclusions:

  • The interplay between polymerization force, actin filaments, and Arp2/3 complex binding dictates self-adaptive cell migration.
  • The developed theory and model provide predictive insights into cell movement dynamics in complex ECMs.
  • Synergistic feedback mechanisms confer powerful, flexible migration and efficient protein utilization.