Source 1primary paper2023
Toolkit/optogenetic actuator
optogenetic actuator
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
This tool is an optogenetic actuator used to control Rho activity with local and reversible effects on cellular contractility. In the cited 2023 study, it was applied to probe DLC1-dependent regulation of Rho signaling at focal adhesions and the plasma membrane.
Usefulness & Problems
Why this is useful
The actuator is useful for perturbing Rho-dependent contractility with spatial and temporal precision using light. In the cited work, this enabled analysis of how DLC1 associates with and dissociates from focal adhesions during reinforcement and relaxation.
Source:
Using a FRET biosensor, we show that DLC1 loss of function leads to global increase in Rho activity and contractility throughout the cell without affecting a striking lamellar RhoA activity band in fibroblasts.
Problem solved
This tool helps address the problem of dissecting local, dynamic regulation of Rho signaling and contractility in living cells. Specifically, it was used to test how DLC1 contributes to tension-linked signaling behavior at focal adhesions rather than only global Rho phenotypes.
Problem links
Need precise spatiotemporal control with light input
DerivedThis tool is an optogenetic actuator used to control Rho activity with local and reversible effects on cellular contractility. In the cited 2023 study, it was applied to probe DLC1-dependent regulation of Rho signaling at focal adhesions and the plasma membrane.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Techniques
No technique tags yet.
Target processes
No target processes tagged yet.
Input: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementoperating role: sensor
The available evidence indicates only that the construct is a light-input optogenetic actuator for controlling Rho activity. No traceable details are provided on construct architecture, cofactors, expression system, delivery method, or illumination protocol.
The supplied evidence does not specify the actuator's molecular components, photoreceptor system, illumination wavelength, kinetic parameters, or quantitative dynamic range. Validation is limited here to a single cited study context focused on DLC1 and focal adhesion biology.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
DLC1 loss of function leads to a global increase in Rho activity and contractility throughout the cell without affecting the lamellar RhoA activity band in fibroblasts.
Using a FRET biosensor, we show that DLC1 loss of function leads to global increase in Rho activity and contractility throughout the cell without affecting a striking lamellar RhoA activity band in fibroblasts.
DLC1 loss of function leads to a global increase in Rho activity and contractility throughout the cell without affecting the lamellar RhoA activity band in fibroblasts.
Using a FRET biosensor, we show that DLC1 loss of function leads to global increase in Rho activity and contractility throughout the cell without affecting a striking lamellar RhoA activity band in fibroblasts.
DLC1 loss of function leads to a global increase in Rho activity and contractility throughout the cell without affecting the lamellar RhoA activity band in fibroblasts.
Using a FRET biosensor, we show that DLC1 loss of function leads to global increase in Rho activity and contractility throughout the cell without affecting a striking lamellar RhoA activity band in fibroblasts.
DLC1 loss of function leads to a global increase in Rho activity and contractility throughout the cell without affecting the lamellar RhoA activity band in fibroblasts.
Using a FRET biosensor, we show that DLC1 loss of function leads to global increase in Rho activity and contractility throughout the cell without affecting a striking lamellar RhoA activity band in fibroblasts.
DLC1 loss of function leads to a global increase in Rho activity and contractility throughout the cell without affecting the lamellar RhoA activity band in fibroblasts.
Using a FRET biosensor, we show that DLC1 loss of function leads to global increase in Rho activity and contractility throughout the cell without affecting a striking lamellar RhoA activity band in fibroblasts.
DLC1 loss of function leads to a global increase in Rho activity and contractility throughout the cell without affecting the lamellar RhoA activity band in fibroblasts.
Using a FRET biosensor, we show that DLC1 loss of function leads to global increase in Rho activity and contractility throughout the cell without affecting a striking lamellar RhoA activity band in fibroblasts.
DLC1 loss of function leads to a global increase in Rho activity and contractility throughout the cell without affecting the lamellar RhoA activity band in fibroblasts.
Using a FRET biosensor, we show that DLC1 loss of function leads to global increase in Rho activity and contractility throughout the cell without affecting a striking lamellar RhoA activity band in fibroblasts.
Local and reversible optogenetic control of contractility shows that DLC1 associates and dissociates with focal adhesions during their reinforcement and relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates/dissociates with FAs during their reinforcement/relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates and dissociates with focal adhesions during their reinforcement and relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates/dissociates with FAs during their reinforcement/relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates and dissociates with focal adhesions during their reinforcement and relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates/dissociates with FAs during their reinforcement/relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates and dissociates with focal adhesions during their reinforcement and relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates/dissociates with FAs during their reinforcement/relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates and dissociates with focal adhesions during their reinforcement and relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates/dissociates with FAs during their reinforcement/relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates and dissociates with focal adhesions during their reinforcement and relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates/dissociates with FAs during their reinforcement/relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates and dissociates with focal adhesions during their reinforcement and relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates/dissociates with FAs during their reinforcement/relaxation.
DLC1 may provide positive feedback that locally increases the rate of Rho activation at focal adhesions experiencing local tension to facilitate focal adhesion disassembly.
This might provide positive feedback that locally increases the rate of Rho activation at FAs that experience local tension to facilitate FA disassembly.
DLC1 may provide positive feedback that locally increases the rate of Rho activation at focal adhesions experiencing local tension to facilitate focal adhesion disassembly.
This might provide positive feedback that locally increases the rate of Rho activation at FAs that experience local tension to facilitate FA disassembly.
DLC1 may provide positive feedback that locally increases the rate of Rho activation at focal adhesions experiencing local tension to facilitate focal adhesion disassembly.
This might provide positive feedback that locally increases the rate of Rho activation at FAs that experience local tension to facilitate FA disassembly.
DLC1 may provide positive feedback that locally increases the rate of Rho activation at focal adhesions experiencing local tension to facilitate focal adhesion disassembly.
This might provide positive feedback that locally increases the rate of Rho activation at FAs that experience local tension to facilitate FA disassembly.
DLC1 may provide positive feedback that locally increases the rate of Rho activation at focal adhesions experiencing local tension to facilitate focal adhesion disassembly.
This might provide positive feedback that locally increases the rate of Rho activation at FAs that experience local tension to facilitate FA disassembly.
DLC1 may provide positive feedback that locally increases the rate of Rho activation at focal adhesions experiencing local tension to facilitate focal adhesion disassembly.
This might provide positive feedback that locally increases the rate of Rho activation at FAs that experience local tension to facilitate FA disassembly.
DLC1 may provide positive feedback that locally increases the rate of Rho activation at focal adhesions experiencing local tension to facilitate focal adhesion disassembly.
This might provide positive feedback that locally increases the rate of Rho activation at FAs that experience local tension to facilitate FA disassembly.
DLC1 operates at both the plasma membrane and focal adhesions to regulate global Rho activity levels at steady state and to amplify local Rho activity at focal adhesions experiencing strong mechanical input.
Our results indicate that DLC1 operates both at the PM and at FAs to regulate global Rho activity levels at steady state, or to amplify local Rho activity at FAs experiencing a strong mechanical input, presumably to induce robust FA disassembly.
DLC1 operates at both the plasma membrane and focal adhesions to regulate global Rho activity levels at steady state and to amplify local Rho activity at focal adhesions experiencing strong mechanical input.
Our results indicate that DLC1 operates both at the PM and at FAs to regulate global Rho activity levels at steady state, or to amplify local Rho activity at FAs experiencing a strong mechanical input, presumably to induce robust FA disassembly.
DLC1 operates at both the plasma membrane and focal adhesions to regulate global Rho activity levels at steady state and to amplify local Rho activity at focal adhesions experiencing strong mechanical input.
Our results indicate that DLC1 operates both at the PM and at FAs to regulate global Rho activity levels at steady state, or to amplify local Rho activity at FAs experiencing a strong mechanical input, presumably to induce robust FA disassembly.
DLC1 operates at both the plasma membrane and focal adhesions to regulate global Rho activity levels at steady state and to amplify local Rho activity at focal adhesions experiencing strong mechanical input.
Our results indicate that DLC1 operates both at the PM and at FAs to regulate global Rho activity levels at steady state, or to amplify local Rho activity at FAs experiencing a strong mechanical input, presumably to induce robust FA disassembly.
DLC1 operates at both the plasma membrane and focal adhesions to regulate global Rho activity levels at steady state and to amplify local Rho activity at focal adhesions experiencing strong mechanical input.
Our results indicate that DLC1 operates both at the PM and at FAs to regulate global Rho activity levels at steady state, or to amplify local Rho activity at FAs experiencing a strong mechanical input, presumably to induce robust FA disassembly.
DLC1 operates at both the plasma membrane and focal adhesions to regulate global Rho activity levels at steady state and to amplify local Rho activity at focal adhesions experiencing strong mechanical input.
Our results indicate that DLC1 operates both at the PM and at FAs to regulate global Rho activity levels at steady state, or to amplify local Rho activity at FAs experiencing a strong mechanical input, presumably to induce robust FA disassembly.
DLC1 operates at both the plasma membrane and focal adhesions to regulate global Rho activity levels at steady state and to amplify local Rho activity at focal adhesions experiencing strong mechanical input.
Our results indicate that DLC1 operates both at the PM and at FAs to regulate global Rho activity levels at steady state, or to amplify local Rho activity at FAs experiencing a strong mechanical input, presumably to induce robust FA disassembly.
In spreading cells at steady state, DLC1 controls the rate of Rho activation rather than its duration at focal adhesions and at the plasma membrane.
In spreading cells at steady state, optogenetic manipulation of Rho activity reveals that DLC1 controls the rate of Rho activation rather than duration, both at FAs and at the plasma membrane (PM).
In spreading cells at steady state, DLC1 controls the rate of Rho activation rather than its duration at focal adhesions and at the plasma membrane.
In spreading cells at steady state, optogenetic manipulation of Rho activity reveals that DLC1 controls the rate of Rho activation rather than duration, both at FAs and at the plasma membrane (PM).
In spreading cells at steady state, DLC1 controls the rate of Rho activation rather than its duration at focal adhesions and at the plasma membrane.
In spreading cells at steady state, optogenetic manipulation of Rho activity reveals that DLC1 controls the rate of Rho activation rather than duration, both at FAs and at the plasma membrane (PM).
In spreading cells at steady state, DLC1 controls the rate of Rho activation rather than its duration at focal adhesions and at the plasma membrane.
In spreading cells at steady state, optogenetic manipulation of Rho activity reveals that DLC1 controls the rate of Rho activation rather than duration, both at FAs and at the plasma membrane (PM).
In spreading cells at steady state, DLC1 controls the rate of Rho activation rather than its duration at focal adhesions and at the plasma membrane.
In spreading cells at steady state, optogenetic manipulation of Rho activity reveals that DLC1 controls the rate of Rho activation rather than duration, both at FAs and at the plasma membrane (PM).
In spreading cells at steady state, DLC1 controls the rate of Rho activation rather than its duration at focal adhesions and at the plasma membrane.
In spreading cells at steady state, optogenetic manipulation of Rho activity reveals that DLC1 controls the rate of Rho activation rather than duration, both at FAs and at the plasma membrane (PM).
In spreading cells at steady state, DLC1 controls the rate of Rho activation rather than its duration at focal adhesions and at the plasma membrane.
In spreading cells at steady state, optogenetic manipulation of Rho activity reveals that DLC1 controls the rate of Rho activation rather than duration, both at FAs and at the plasma membrane (PM).
Approval Evidence
1 source1 linked approval claimfirst-pass slug optogenetic-actuator
an optogenetic actuator to control Rho activity
Source:
localization dynamicssupports
Local and reversible optogenetic control of contractility shows that DLC1 associates and dissociates with focal adhesions during their reinforcement and relaxation.
Local and reversible optogenetic control of contractility shows that DLC1 associates/dissociates with FAs during their reinforcement/relaxation.
Source:
Comparisons
Source-backed strengths
The reported strengths are local and reversible optical control of contractility and suitability for probing spatiotemporal Rho regulation. Its application supported mechanistic observations linking DLC1 dynamics to focal adhesion reinforcement and relaxation.
Compared with artificial differentiation system
optogenetic actuator and artificial differentiation system address a similar problem space.
Shared frame: same top-level item type; shared mechanisms: optogenetic control; same primary input modality: light
Compared with split recombinases
optogenetic actuator and split recombinases address a similar problem space.
Shared frame: same top-level item type; shared mechanisms: optogenetic control; same primary input modality: light
Compared with TRIM21-nanobody chimeras
optogenetic actuator and TRIM21-nanobody chimeras address a similar problem space.
Shared frame: same top-level item type; shared mechanisms: optogenetic control; same primary input modality: light
Ranked Citations
- 1.