Source 1primary paper2023Communications Physics
Toolkit/one-dimensional active gel model
one-dimensional active gel model
Also known as: active gel model
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
The one-dimensional active gel model is a theoretical computational framework for contractile cell migration that incorporates the tendency of myosin II to assemble into minifilaments. It predicts bistability between sessile and motile cell states and models how optogenetic activation or inhibition of contractility can switch between these states.
Usefulness & Problems
Why this is useful
This model is useful for analyzing how adhesion, contractility, and myosin II minifilament assembly shape transitions between non-migratory and migratory cell behaviors. It also provides a theoretical framework for evaluating light-driven perturbations of contractility in contractile cells.
Problem solved
It addresses the problem of explaining and predicting when contractile cells exhibit sessile versus motile states under coupled mechanical regulation by adhesion and contractility. It also specifically tackles how optogenetic activation or inhibition of contractility could induce switching between these states at realistic parameter values.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete computational method used to design, rank, or analyze an engineered system.
Mechanisms
active gel mechanicsbistability between sessile and motile statescontractility modulationmyosin ii minifilament assemblyTechniques
Computational DesignTarget processes
No target processes tagged yet.
Input: Light
Implementation Constraints
Implementation is described only at the level of a one-dimensional theoretical active gel model for contractile cells. The model reflects myosin II minifilament assembly and is used to simulate optogenetic activation or inhibition of contractility, but the provided evidence does not report software, equations, parameter sets, or experimental delivery details.
The supplied evidence describes this tool as a theoretical one-dimensional model, so its validation is limited to model-based predictions rather than direct experimental demonstration in the provided record. The evidence does not specify numerical implementation details, parameter inference procedures, or performance across multiple cell types and geometries.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2primary paper2022arXiv (Cornell University)
Ranked Claims
Actin polymerization alone can switch migration direction only at high strength.
show that actin polymerization alone can affect a switch in direction only at high strength
Actin polymerization alone can switch migration direction only at high strength.
show that actin polymerization alone can affect a switch in direction only at high strength
Actin polymerization alone can switch migration direction only at high strength.
show that actin polymerization alone can affect a switch in direction only at high strength
Actin polymerization alone can switch migration direction only at high strength.
show that actin polymerization alone can affect a switch in direction only at high strength
Actin polymerization alone can switch migration direction only at high strength.
show that actin polymerization alone can affect a switch in direction only at high strength
Actin polymerization alone can switch migration direction only at high strength.
show that actin polymerization alone can affect a switch in direction only at high strength
Actin polymerization alone can switch migration direction only at high strength.
show that actin polymerization alone can affect a switch in direction only at high strength
A one-dimensional active gel model predicts bistability between sessile and motile cell states when adhesion and contractility are sufficiently large and balanced.
Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance.
A one-dimensional active gel model predicts bistability between sessile and motile cell states when adhesion and contractility are sufficiently large and balanced.
Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance.
A one-dimensional active gel model predicts bistability between sessile and motile cell states when adhesion and contractility are sufficiently large and balanced.
Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance.
A one-dimensional active gel model predicts bistability between sessile and motile cell states when adhesion and contractility are sufficiently large and balanced.
Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance.
A one-dimensional active gel model predicts bistability between sessile and motile cell states when adhesion and contractility are sufficiently large and balanced.
Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance.
A one-dimensional active gel model predicts bistability between sessile and motile cell states when adhesion and contractility are sufficiently large and balanced.
Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance.
A one-dimensional active gel model predicts bistability between sessile and motile cell states when adhesion and contractility are sufficiently large and balanced.
Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance.
Optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter values.
We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility
Optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter values.
We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility
Optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter values.
We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility
Optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter values.
We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility
Optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter values.
We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility
Optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter values.
We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility
Optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter values.
We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility
The model indicates that optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter ranges.
We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments.
The model indicates that optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter ranges.
We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments.
The model indicates that optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter ranges.
We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments.
The model indicates that optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter ranges.
We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments.
The model indicates that optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter ranges.
We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments.
The model indicates that optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter ranges.
We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments.
The model indicates that optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter ranges.
We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments.
The model predicts required activation strengths and initiation times for switching.
We also predict the required activation strengths and initiation times.
The model predicts required activation strengths and initiation times for switching.
We also predict the required activation strengths and initiation times.
The model predicts required activation strengths and initiation times for switching.
We also predict the required activation strengths and initiation times.
The model predicts required activation strengths and initiation times for switching.
We also predict the required activation strengths and initiation times.
The model predicts required activation strengths and initiation times for switching.
We also predict the required activation strengths and initiation times.
The model predicts required activation strengths and initiation times for switching.
We also predict the required activation strengths and initiation times.
The model predicts required activation strengths and initiation times for switching.
We also predict the required activation strengths and initiation times.
The one-dimensional active gel model predicts bistability between sessile and motile solutions.
This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions.
The one-dimensional active gel model predicts bistability between sessile and motile solutions.
This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions.
The one-dimensional active gel model predicts bistability between sessile and motile solutions.
This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions.
The one-dimensional active gel model predicts bistability between sessile and motile solutions.
This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions.
The one-dimensional active gel model predicts bistability between sessile and motile solutions.
This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions.
The one-dimensional active gel model predicts bistability between sessile and motile solutions.
This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions.
The one-dimensional active gel model predicts bistability between sessile and motile solutions.
This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions.
Approval Evidence
2 sources6 linked approval claimsfirst-pass slug one-dimensional-active-gel-model
Here we theoretically analyze this situation using a one-dimensional active gel model that reflects the property of myosin II to assemble into minifilaments.
Source:
Here we analyze this situation theoretically using a one-dimensional active gel model
Source:
comparisonsupports
Actin polymerization alone can switch migration direction only at high strength.
show that actin polymerization alone can affect a switch in direction only at high strength
Source:
model predictionsupports
A one-dimensional active gel model predicts bistability between sessile and motile cell states when adhesion and contractility are sufficiently large and balanced.
Our model predicts bistability between sessile and motile solutions when cell adhesion and contractility are sufficiently large and in balance.
Source:
model predictionsupports
Optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter values.
We show that one can switch between the different states at realistic parameter values via optogenetic activation or inhibition of contractility
Source:
model predictionsupports
The model indicates that optogenetic activation or inhibition of contractility can switch cells between sessile and motile states at realistic parameter ranges.
We then show that one can switch between these two states at realistic parameter ranges via optogenetic activation or inhibition of contractility, in agreement with recent experiments.
Source:
model predictionsupports
The model predicts required activation strengths and initiation times for switching.
We also predict the required activation strengths and initiation times.
Source:
model predictionsupports
The one-dimensional active gel model predicts bistability between sessile and motile solutions.
This physically simple and transparent, but nonlinear and thermodynamically rigorous model predicts bistability between sessile and motile solutions.
Source:
Comparisons
Source-backed strengths
The model explicitly reflects the property of myosin II to assemble into minifilaments, linking contractility to a biologically motivated active-gel description. It predicts bistability when adhesion and contractility are sufficiently large and balanced, and it further predicts that optogenetic modulation of contractility can switch cells between sessile and motile states. The cited comparison also indicates that actin polymerization alone switches migration direction only at high strength, highlighting the model's emphasis on contractility-based control.
Ranked Citations
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