Toolkit/lyso-ChR2
lyso-ChR2
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Here, we constructed lysosome-localized optogenetic actuators, named lyso-NpHR3.0, lyso-ArchT, and lyso-ChR2, to achieve optogenetic manipulation of lysosomes. Notably, lyso-ChR2 activation induces autophagy through the mTOR pathway, promotes Aβ clearance in an autophagy-dependent manner in cellular models, and alleviates Aβ-induced paralysis in the Caenorhabditis elegans model of Alzheimer's disease.
Usefulness & Problems
Why this is useful
lyso-ChR2 is a lysosome-localized optogenetic actuator used to manipulate lysosomal physiology with light. The abstract further states that its activation induces autophagy through the mTOR pathway and promotes amyloid beta clearance.; optogenetic manipulation of lysosomes; inducing autophagy through the mTOR pathway; promoting Aβ clearance; testing lysosome-directed intervention in cellular and animal disease models
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lyso-ChR2 is a lysosome-localized optogenetic actuator used to manipulate lysosomal physiology with light. The abstract further states that its activation induces autophagy through the mTOR pathway and promotes amyloid beta clearance.
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optogenetic manipulation of lysosomes
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inducing autophagy through the mTOR pathway
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promoting Aβ clearance
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testing lysosome-directed intervention in cellular and animal disease models
Problem solved
It provides a dynamic way to regulate lysosomal physiology and to test how lysosomal activation affects autophagy and amyloid beta handling.; lack of methods to dynamically regulate lysosomal function in living cells or animals; need for a dynamic method to probe links between lysosomal physiology, autophagy, and amyloid beta clearance
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It provides a dynamic way to regulate lysosomal physiology and to test how lysosomal activation affects autophagy and amyloid beta handling.
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lack of methods to dynamically regulate lysosomal function in living cells or animals
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need for a dynamic method to probe links between lysosomal physiology, autophagy, and amyloid beta clearance
Problem links
lack of methods to dynamically regulate lysosomal function in living cells or animals
LiteratureIt provides a dynamic way to regulate lysosomal physiology and to test how lysosomal activation affects autophagy and amyloid beta handling.
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It provides a dynamic way to regulate lysosomal physiology and to test how lysosomal activation affects autophagy and amyloid beta handling.
need for a dynamic method to probe links between lysosomal physiology, autophagy, and amyloid beta clearance
LiteratureIt provides a dynamic way to regulate lysosomal physiology and to test how lysosomal activation affects autophagy and amyloid beta handling.
Source:
It provides a dynamic way to regulate lysosomal physiology and to test how lysosomal activation affects autophagy and amyloid beta handling.
Published Workflows
Optogenetic manipulation of lysosomal physiology and autophagy-dependent clearance of amyloid beta.
2024Objective: Construct lysosome-localized optogenetic actuators to dynamically regulate lysosomal physiology and test whether lysosomal optical control can drive autophagy and amyloid beta clearance in living cells and animals.
Why it works: The paper's logic is that lysosome-localized optogenetic actuators allow dynamic, light-dependent perturbation of lysosomal physiological parameters, enabling causal testing of how lysosomal state affects autophagy and amyloid beta clearance.
Stages
- 1.Construction of lysosome-localized optogenetic actuators(library_build)
This stage creates the engineered tools needed for dynamic optical perturbation of lysosomal function.
Selection: Build lysosome-localized actuators lyso-NpHR3.0, lyso-ArchT, and lyso-ChR2 for optogenetic manipulation of lysosomes.
- 2.Functional characterization of lysosomal physiological control in living cells(functional_characterization)
This stage establishes that the engineered actuators actually modulate lysosomal physiology in living cells before disease-relevant applications are tested.
Selection: Test whether the new actuators enable light-dependent control of lysosomal membrane potential, pH, hydrolase activity, degradation, and Ca2+ dynamics in living cells.
- 3.Application testing of lyso-ChR2 in autophagy and amyloid beta clearance(confirmatory_validation)
This stage tests whether lysosomal optical control translates into mechanistic and disease-relevant cellular outcomes.
Selection: Use lyso-ChR2 to test autophagy induction through the mTOR pathway and autophagy-dependent Aβ clearance in cellular models.
- 4.In vivo validation in a Caenorhabditis elegans Alzheimer's disease model(in_vivo_validation)
This stage extends cellular findings to an animal disease model.
Selection: Test whether lyso-ChR2 alleviates Aβ-induced paralysis in a Caenorhabditis elegans model of Alzheimer's disease.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Mechanisms
Degradationlight-dependent modulation of lysosomal membrane potentialmtor-pathway-mediated autophagy inductionoptogenetic ion-channel activationTechniques
No technique tags yet.
Target processes
degradationInput: Light
Implementation Constraints
Use requires expression of a lysosome-localized optogenetic construct and light stimulation in living cells or animals.; requires light activation; requires lysosome-localized actuator expression
Needs compatible illumination hardware and optical access. Independent follow-up evidence is still limited. Validation breadth across biological contexts is still narrow. Independent reuse still looks limited, so the evidence base may be fragile. No canonical validation observations are stored yet, so context-specific performance remains under-specified.
Validation
Supporting Sources
Ranked Claims
lyso-ChR2 activation promotes Aβ clearance in an autophagy-dependent manner in cellular models.
promotes Aβ clearance in an autophagy-dependent manner in cellular models
lyso-ChR2 alleviates Aβ-induced paralysis in the Caenorhabditis elegans model of Alzheimer's disease.
and alleviates Aβ-induced paralysis in the Caenorhabditis elegans model of Alzheimer's disease
lyso-ChR2 activation induces autophagy through the mTOR pathway.
Notably, lyso-ChR2 activation induces autophagy through the mTOR pathway
lyso-NpHR3.0, lyso-ArchT, and lyso-ChR2 are lysosome-localized optogenetic actuators constructed to achieve optogenetic manipulation of lysosomes.
Here, we constructed lysosome-localized optogenetic actuators, named lyso-NpHR3.0, lyso-ArchT, and lyso-ChR2, to achieve optogenetic manipulation of lysosomes.
The lysosome-localized optogenetic actuators enable light-dependent control of lysosomal membrane potential, pH, hydrolase activity, degradation, and Ca2+ dynamics in living cells.
These new actuators enable light-dependent control of lysosomal membrane potential, pH, hydrolase activity, degradation, and Ca2+ dynamics in living cells.
Lysosomal optogenetic actuators provide a method to dynamically regulate lysosomal physiology and function in living cells and animals.
Our lysosomal optogenetic actuators supplement the optogenetic toolbox and provide a method to dynamically regulate lysosomal physiology and function in living cells and animals.
Approval Evidence
Here, we constructed lysosome-localized optogenetic actuators, named lyso-NpHR3.0, lyso-ArchT, and lyso-ChR2, to achieve optogenetic manipulation of lysosomes. Notably, lyso-ChR2 activation induces autophagy through the mTOR pathway, promotes Aβ clearance in an autophagy-dependent manner in cellular models, and alleviates Aβ-induced paralysis in the Caenorhabditis elegans model of Alzheimer's disease.
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lyso-ChR2 activation promotes Aβ clearance in an autophagy-dependent manner in cellular models.
promotes Aβ clearance in an autophagy-dependent manner in cellular models
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lyso-ChR2 alleviates Aβ-induced paralysis in the Caenorhabditis elegans model of Alzheimer's disease.
and alleviates Aβ-induced paralysis in the Caenorhabditis elegans model of Alzheimer's disease
Source:
lyso-ChR2 activation induces autophagy through the mTOR pathway.
Notably, lyso-ChR2 activation induces autophagy through the mTOR pathway
Source:
lyso-NpHR3.0, lyso-ArchT, and lyso-ChR2 are lysosome-localized optogenetic actuators constructed to achieve optogenetic manipulation of lysosomes.
Here, we constructed lysosome-localized optogenetic actuators, named lyso-NpHR3.0, lyso-ArchT, and lyso-ChR2, to achieve optogenetic manipulation of lysosomes.
Source:
The lysosome-localized optogenetic actuators enable light-dependent control of lysosomal membrane potential, pH, hydrolase activity, degradation, and Ca2+ dynamics in living cells.
These new actuators enable light-dependent control of lysosomal membrane potential, pH, hydrolase activity, degradation, and Ca2+ dynamics in living cells.
Source:
Lysosomal optogenetic actuators provide a method to dynamically regulate lysosomal physiology and function in living cells and animals.
Our lysosomal optogenetic actuators supplement the optogenetic toolbox and provide a method to dynamically regulate lysosomal physiology and function in living cells and animals.
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Comparisons
Source-stated alternatives
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
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The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Source-backed strengths
lysosome-localized optogenetic actuator; linked in the abstract to autophagy induction through the mTOR pathway; associated with Aβ clearance in cellular models; associated with alleviation of Aβ-induced paralysis in a Caenorhabditis elegans Alzheimer's disease model
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lysosome-localized optogenetic actuator
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linked in the abstract to autophagy induction through the mTOR pathway
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associated with Aβ clearance in cellular models
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associated with alleviation of Aβ-induced paralysis in a Caenorhabditis elegans Alzheimer's disease model
Compared with lyso-ArchT
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Shared frame: source-stated alternative in extracted literature
Strengths here: lysosome-localized optogenetic actuator; linked in the abstract to autophagy induction through the mTOR pathway; associated with Aβ clearance in cellular models.
Source:
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Compared with lyso-NpHR3.0
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Shared frame: source-stated alternative in extracted literature
Strengths here: lysosome-localized optogenetic actuator; linked in the abstract to autophagy induction through the mTOR pathway; associated with Aβ clearance in cellular models.
Source:
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Compared with optogenetic
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Shared frame: source-stated alternative in extracted literature
Strengths here: lysosome-localized optogenetic actuator; linked in the abstract to autophagy induction through the mTOR pathway; associated with Aβ clearance in cellular models.
Source:
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Compared with optogenetic actuator
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Shared frame: source-stated alternative in extracted literature
Strengths here: lysosome-localized optogenetic actuator; linked in the abstract to autophagy induction through the mTOR pathway; associated with Aβ clearance in cellular models.
Source:
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Compared with optogenetic actuators
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Shared frame: source-stated alternative in extracted literature
Strengths here: lysosome-localized optogenetic actuator; linked in the abstract to autophagy induction through the mTOR pathway; associated with Aβ clearance in cellular models.
Source:
The same paper presents lyso-NpHR3.0 and lyso-ArchT as related lysosomal optogenetic actuators.
Ranked Citations
- 1.