Toolkit/CRY2-mCherry-Drosophila β-catenin optogenetic switch

CRY2-mCherry-Drosophila β-catenin optogenetic switch

Multi-Component Switch·Research·Since 2017

Also known as: Cryptochrome 2 (CRY2)-mCherry-Drosophila β-catenin fusion protein

Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.

Summary

The CRY2-mCherry-Drosophila β-catenin optogenetic switch is a fusion protein comprising Arabidopsis thaliana CRY2, mCherry, and Drosophila β-catenin. Blue light induces oligomerization of the fusion protein, which inhibits downstream Wnt signaling in vitro and in vivo and enables temporal inactivation of β-catenin.

Usefulness & Problems

Why this is useful

This tool enables light-controlled perturbation of β-catenin/Wnt signaling with temporal precision in vitro and in vivo. The associated study further indicates that coupling this optogenetic switch with light-sheet microscopy supports precise temporal regulation studies of signaling pathways and cellular processes in vivo.

Source:

Bringing the two approaches together allows unparalleled precision into the temporal regulation of signaling pathways and cellular processes in vivo .

Problem solved

It addresses the need to acutely and reversibly inactivate β-catenin during development rather than relying only on static genetic perturbations. In the cited work, temporal inactivation was used to test when Wnt signaling is required for Drosophila pattern formation and later developmental maintenance.

Taxonomy & Function

Primary hierarchy

Mechanism Branch

Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.

Techniques

No technique tags yet.

Target processes

signaling

Input: Light

Implementation Constraints

The construct is formed by fusing Arabidopsis thaliana CRY2 to mCherry fluorescent protein and Drosophila β-catenin. Blue light is the stated input, and the cited work used the switch together with light-sheet microscopy for in vivo temporal perturbation studies.

The provided evidence is limited to a single 2017 source and does not report quantitative performance metrics such as activation wavelength range, kinetics, reversibility, dynamic range, or expression-dependent effects. Independent replication and validation outside the reported Drosophila/Wnt context are not documented in the supplied evidence.

Validation

Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication

Supporting Sources

Ranked Claims

Claim 1biological conclusionsupports2017Source 1needs review

Temporal inactivation of β-catenin confirmed that Wnt signaling is required for Drosophila pattern formation and for maintenance later in development.

Temporal inactivation of β–catenin confirmed that Wnt signaling is required not only for Drosophila pattern formation, but also for maintenance later in development.
Claim 2biological conclusionsupports2017Source 1needs review

Temporal inactivation of β-catenin confirmed that Wnt signaling is required for Drosophila pattern formation and for maintenance later in development.

Temporal inactivation of β–catenin confirmed that Wnt signaling is required not only for Drosophila pattern formation, but also for maintenance later in development.
Claim 3biological conclusionsupports2017Source 1needs review

Temporal inactivation of β-catenin confirmed that Wnt signaling is required for Drosophila pattern formation and for maintenance later in development.

Temporal inactivation of β–catenin confirmed that Wnt signaling is required not only for Drosophila pattern formation, but also for maintenance later in development.
Claim 4biological conclusionsupports2017Source 1needs review

Temporal inactivation of β-catenin confirmed that Wnt signaling is required for Drosophila pattern formation and for maintenance later in development.

Temporal inactivation of β–catenin confirmed that Wnt signaling is required not only for Drosophila pattern formation, but also for maintenance later in development.
Claim 5biological conclusionsupports2017Source 1needs review

Temporal inactivation of β-catenin confirmed that Wnt signaling is required for Drosophila pattern formation and for maintenance later in development.

Temporal inactivation of β–catenin confirmed that Wnt signaling is required not only for Drosophila pattern formation, but also for maintenance later in development.
Claim 6biological conclusionsupports2017Source 1needs review

Temporal inactivation of β-catenin confirmed that Wnt signaling is required for Drosophila pattern formation and for maintenance later in development.

Temporal inactivation of β–catenin confirmed that Wnt signaling is required not only for Drosophila pattern formation, but also for maintenance later in development.
Claim 7biological conclusionsupports2017Source 1needs review

Temporal inactivation of β-catenin confirmed that Wnt signaling is required for Drosophila pattern formation and for maintenance later in development.

Temporal inactivation of β–catenin confirmed that Wnt signaling is required not only for Drosophila pattern formation, but also for maintenance later in development.
Claim 8mechanism of actionsupports2017Source 1needs review

Blue light illumination causes oligomerization of the CRY2-mCherry-Drosophila β-catenin fusion protein and inhibits downstream Wnt signaling in vitro and in vivo.

Blue light illumination caused oligomerization of the fusion protein and inhibited downstream Wnt signaling in vitro and in vivo .
Claim 9mechanism of actionsupports2017Source 1needs review

Blue light illumination causes oligomerization of the CRY2-mCherry-Drosophila β-catenin fusion protein and inhibits downstream Wnt signaling in vitro and in vivo.

Blue light illumination caused oligomerization of the fusion protein and inhibited downstream Wnt signaling in vitro and in vivo .
Claim 10mechanism of actionsupports2017Source 1needs review

Blue light illumination causes oligomerization of the CRY2-mCherry-Drosophila β-catenin fusion protein and inhibits downstream Wnt signaling in vitro and in vivo.

Blue light illumination caused oligomerization of the fusion protein and inhibited downstream Wnt signaling in vitro and in vivo .
Claim 11mechanism of actionsupports2017Source 1needs review

Blue light illumination causes oligomerization of the CRY2-mCherry-Drosophila β-catenin fusion protein and inhibits downstream Wnt signaling in vitro and in vivo.

Blue light illumination caused oligomerization of the fusion protein and inhibited downstream Wnt signaling in vitro and in vivo .
Claim 12mechanism of actionsupports2017Source 1needs review

Blue light illumination causes oligomerization of the CRY2-mCherry-Drosophila β-catenin fusion protein and inhibits downstream Wnt signaling in vitro and in vivo.

Blue light illumination caused oligomerization of the fusion protein and inhibited downstream Wnt signaling in vitro and in vivo .
Claim 13mechanism of actionsupports2017Source 1needs review

Blue light illumination causes oligomerization of the CRY2-mCherry-Drosophila β-catenin fusion protein and inhibits downstream Wnt signaling in vitro and in vivo.

Blue light illumination caused oligomerization of the fusion protein and inhibited downstream Wnt signaling in vitro and in vivo .
Claim 14mechanism of actionsupports2017Source 1needs review

Blue light illumination causes oligomerization of the CRY2-mCherry-Drosophila β-catenin fusion protein and inhibits downstream Wnt signaling in vitro and in vivo.

Blue light illumination caused oligomerization of the fusion protein and inhibited downstream Wnt signaling in vitro and in vivo .
Claim 15method capabilitysupports2017Source 1needs review

Coupling optogenetics and light-sheet microscopy allows precise temporal regulation studies of signaling pathways and cellular processes in vivo.

Bringing the two approaches together allows unparalleled precision into the temporal regulation of signaling pathways and cellular processes in vivo .
Claim 16method capabilitysupports2017Source 1needs review

Coupling optogenetics and light-sheet microscopy allows precise temporal regulation studies of signaling pathways and cellular processes in vivo.

Bringing the two approaches together allows unparalleled precision into the temporal regulation of signaling pathways and cellular processes in vivo .
Claim 17method capabilitysupports2017Source 1needs review

Coupling optogenetics and light-sheet microscopy allows precise temporal regulation studies of signaling pathways and cellular processes in vivo.

Bringing the two approaches together allows unparalleled precision into the temporal regulation of signaling pathways and cellular processes in vivo .
Claim 18method capabilitysupports2017Source 1needs review

Coupling optogenetics and light-sheet microscopy allows precise temporal regulation studies of signaling pathways and cellular processes in vivo.

Bringing the two approaches together allows unparalleled precision into the temporal regulation of signaling pathways and cellular processes in vivo .
Claim 19method capabilitysupports2017Source 1needs review

Coupling optogenetics and light-sheet microscopy allows precise temporal regulation studies of signaling pathways and cellular processes in vivo.

Bringing the two approaches together allows unparalleled precision into the temporal regulation of signaling pathways and cellular processes in vivo .
Claim 20method capabilitysupports2017Source 1needs review

Coupling optogenetics and light-sheet microscopy allows precise temporal regulation studies of signaling pathways and cellular processes in vivo.

Bringing the two approaches together allows unparalleled precision into the temporal regulation of signaling pathways and cellular processes in vivo .
Claim 21method capabilitysupports2017Source 1needs review

Coupling optogenetics and light-sheet microscopy allows precise temporal regulation studies of signaling pathways and cellular processes in vivo.

Bringing the two approaches together allows unparalleled precision into the temporal regulation of signaling pathways and cellular processes in vivo .

Approval Evidence

1 source2 linked approval claimsfirst-pass slug cry2-mcherry-drosophila-catenin-optogenetic-switch
Cryptochrome 2 (CRY2) from Arabidopsis Thaliana was fused to mCherry fluorescent protein and Drosophila β–catenin to form an easy to visualize optogenetic switch.

Source:

biological conclusionsupports

Temporal inactivation of β-catenin confirmed that Wnt signaling is required for Drosophila pattern formation and for maintenance later in development.

Temporal inactivation of β–catenin confirmed that Wnt signaling is required not only for Drosophila pattern formation, but also for maintenance later in development.

Source:

mechanism of actionsupports

Blue light illumination causes oligomerization of the CRY2-mCherry-Drosophila β-catenin fusion protein and inhibits downstream Wnt signaling in vitro and in vivo.

Blue light illumination caused oligomerization of the fusion protein and inhibited downstream Wnt signaling in vitro and in vivo .

Source:

Comparisons

Source-backed strengths

The fusion is directly visualizable because it contains mCherry, and the reported response is triggered by blue light. The source reports inhibition of downstream Wnt signaling in both in vitro and in vivo settings, supporting utility across experimental contexts.

Ranked Citations

  1. 1.

    Extracted from this source document.