Source 1primary paper2020Science Advances
Toolkit/optogenetically driven repositioning of lysosomes
optogenetically driven repositioning of lysosomes
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Optogenetically driven repositioning of lysosomes is a light-controlled perturbation method used to move lysosomes and test their causal role in endoplasmic reticulum remodeling. In the cited 2020 study, chemo- and optogenetically driven lysosome repositioning was used to validate a causal link between lysosome positioning and ER network organization.
Usefulness & Problems
Why this is useful
This method is useful for causally perturbing lysosome localization with temporal control to assess how lysosome positioning influences ER tubule distribution and global ER morphology. The cited work specifically used it to interrogate lysosome-dependent ER remodeling in the context of changing nutritional status and axonal extension-related cell biology.
Problem solved
It addresses the problem that correlative observations between lysosome movement and ER remodeling do not establish causality. By experimentally repositioning lysosomes, the method enables direct testing of whether lysosomes actively drive ER tubule elongation, connection, and large-scale ER redistribution.
Problem links
Need precise spatiotemporal control with light input
DerivedOptogenetically driven repositioning of lysosomes is a light-controlled perturbation method used to move lysosomes and test their causal role in endoplasmic reticulum (ER) remodeling. In the cited study, optogenetic lysosome repositioning led to redistribution of ER tubules and changes in global ER morphology.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete method used to build, optimize, or evolve 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: builder
The available evidence indicates that the method requires an optogenetic system capable of driving lysosome repositioning, but no specific photoreceptor, effector domain, or illumination parameters are provided. The same study also used chemogenetic repositioning as a complementary perturbation, suggesting that orthogonal control strategies were paired for causal testing.
The provided evidence does not specify the optogenetic actuator, wavelengths, construct architecture, dynamic range, or quantitative performance of lysosome repositioning. Validation is currently limited to the cited study, and the evidence here does not establish generality across cell types, organisms, or experimental platforms.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Approval Evidence
1 source5 linked approval claimsfirst-pass slug optogenetically-driven-repositioning-of-lysosomes
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes
Source:
disease or phenotype implicationsupports
Dysfunction in the lysosome-regulated ER remodeling mechanism during axonal extension may lead to axonal growth defects.
Dysfunction in this mechanism during axonal extension may lead to axonal growth defects.
Source:
mechanistic rolesupports
Anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection.
Source:
mechanistic rolesupports
ER remodeling is actively driven by lysosomes following lysosome repositioning in response to changes in nutritional status.
Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status
Source:
perturbation effectsupports
Chemo- and optogenetically driven repositioning of lysosomes leads to redistribution of ER tubules and changes in global ER morphology.
We validate this causal link via the chemo- and optogenetically driven repositioning of lysosomes, which leads to both a redistribution of the ER tubules and a change of its global morphology.
Source:
regulatory rolesupports
Lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Therefore, lysosomes sense metabolic change in the cell and regulate ER tubule distribution accordingly.
Source:
Comparisons
Source-backed strengths
The main strength supported by the evidence is causal validation: the study states that the lysosome-ER link was validated through chemo- and optogenetically driven lysosome repositioning. The biological effect tested is mechanistically relevant because the same study reports that lysosome anchorage to ER growth tips is critical for ER tubule elongation and connection.
optogenetically driven repositioning of lysosomes and Method for efficient synthesis of phycocyanobilin in cultured mammalian cells address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Strengths here: may avoid an exogenous cofactor requirement.
Compared with optogenetic
optogenetically driven repositioning of lysosomes and optogenetic address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Compared with reversible optogenetic unmasking-masking of Ct residues
optogenetically driven repositioning of lysosomes and reversible optogenetic unmasking-masking of Ct residues address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Ranked Citations
- 1.