Source 1primary paper2020Science Advances
Toolkit/chemogenetically driven repositioning of lysosomes
chemogenetically driven repositioning of lysosomes
Also known as: chemo-driven repositioning of lysosomes
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Chemogenetically driven repositioning of lysosomes is an experimental perturbation used to causally alter lysosome localization and test how lysosome positioning regulates endoplasmic reticulum remodeling. In the cited 2020 Science Advances study, chemo- and optogenetically driven lysosome repositioning was used to validate a causal link between lysosome movement and ER network organization.
Usefulness & Problems
Why this is useful
This method is useful for dissecting whether lysosome positioning actively drives ER tubule redistribution and global ER morphology rather than merely correlating with them. The cited study used it to probe lysosome-regulated ER remodeling in the context of nutritional-state-dependent lysosome repositioning and axonal extension.
Problem solved
It addresses the problem of establishing causality between organelle positioning and ER network architecture. Specifically, it enables perturbation of lysosome localization to test whether lysosome anchorage and movement contribute to ER tubule elongation, connection, and large-scale ER distribution.
Problem links
Need precise spatiotemporal control with light input
DerivedChemogenetically driven repositioning of lysosomes is an engineering perturbation used to causally manipulate lysosome localization and assess its effects on endoplasmic reticulum organization. In the cited study, chemo- and optogenetically driven lysosome repositioning caused 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.
Mechanisms
chemically induced repositioningchemically induced repositioningoptogenetic control of organelle positioningoptogenetic control of organelle positioningTechniques
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 approach was implemented as a chemogenetic and optogenetic lysosome repositioning perturbation in a study of ER organization. However, the supplied material does not report construct design, expression system, delivery method, cofactors, or illumination parameters.
The provided evidence does not specify the molecular constructs, ligands, light-responsive modules, wavelengths, or quantitative performance metrics of the chemogenetic system. Validation is currently supported here by a single primary study focused on ER remodeling, so generality to other cell types or organelle interactions is not established from the supplied evidence.
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 chemogenetically-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 perturbation: lysosomes were repositioned by chemo- and optogenetic means to validate their active role in ER remodeling. The associated study links lysosome repositioning to ER tubule redistribution, global ER morphology, and ER growth-tip behavior.
chemogenetically 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
chemogenetically 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
chemogenetically 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.