Source 1primary paper2017Nucleic Acids Research
Toolkit/FKF1/GIGANTEA light-inducible transcription system
FKF1/GIGANTEA light-inducible transcription system
Also known as: FKF1/GI, split FKF1/GI dimerized Gal4-VP16 transcriptional system
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
The FKF1/GIGANTEA light-inducible transcription system is an optogenetic multi-component switch for mammalian cells built from the Arabidopsis photoreceptor FKF1 and its binding partner GIGANTEA. In an optimized split FKF1/GI dimerized Gal4-VP16 configuration, light induces transcriptional activation by reconstituting a functional transcriptional regulator.
Usefulness & Problems
Why this is useful
This system provides light-dependent control of transcription in mammalian cells using plant-derived interaction partners adapted for optogenetic regulation. The cited study presents the optimized FKF1/GI system as widely applicable for inducible transcriptional control in this context.
Source:
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
Source:
In addition, we have improved the CRY2/CIB1-based light-inducible transcription with split construct optimization.
Source:
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Problem solved
It addresses the need for externally controllable transcription systems in mammalian cells that can be activated by light rather than constitutive expression alone. The reported engineering specifically sought to improve light-triggered transcriptional induction from FKF1/GI-based constructs.
Source:
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
Problem links
Need precise spatiotemporal control with light input
DerivedThe FKF1/GIGANTEA light-inducible transcription system is an optogenetic, multi-component switch for mammalian cells built from the Arabidopsis photoreceptor FKF1 and its binding partner GIGANTEA. In an optimized split FKF1/GI dimerized Gal4-VP16 configuration, light triggers transcriptional induction.
Need tighter control over gene expression timing or amplitude
DerivedThe FKF1/GIGANTEA light-inducible transcription system is an optogenetic, multi-component switch for mammalian cells built from the Arabidopsis photoreceptor FKF1 and its binding partner GIGANTEA. In an optimized split FKF1/GI dimerized Gal4-VP16 configuration, light triggers transcriptional induction.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
HeterodimerizationHeterodimerizationlight-induced heterodimerizationlight-induced heterodimerizationtranscriptional activation via split transcription factor reconstitutiontranscriptional activation via split transcription factor reconstitutionTechniques
No technique tags yet.
Target processes
transcriptionInput: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: multi component delivery burdenimplementation constraint: spectral hardware requirementoperating role: regulatorswitch architecture: multi componentswitch architecture: recruitmentswitch architecture: split
The system uses Arabidopsis FKF1 and GIGANTEA components in mammalian cells and was engineered as a split FKF1/GI dimerized Gal4-VP16 transcriptional system. The evidence supports the use of FKF1 mutagenesis together with split construct optimization, but it does not specify exact mutations, construct boundaries, illumination parameters, or delivery methods.
The supplied evidence does not provide quantitative performance metrics, kinetic parameters, background activity, wavelength specifications, or comparisons against alternative systems beyond noting optimization. Validation is only described in mammalian cells from a single cited study, so breadth across cell types and independent replication is not established here.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
CRY2/CIB1-based light-inducible transcription was improved by split construct optimization in mammalian cells.
In addition, we have improved the CRY2/CIB1-based light-inducible transcription with split construct optimization.
CRY2/CIB1-based light-inducible transcription was improved by split construct optimization in mammalian cells.
In addition, we have improved the CRY2/CIB1-based light-inducible transcription with split construct optimization.
CRY2/CIB1-based light-inducible transcription was improved by split construct optimization in mammalian cells.
In addition, we have improved the CRY2/CIB1-based light-inducible transcription with split construct optimization.
CRY2/CIB1-based light-inducible transcription was improved by split construct optimization in mammalian cells.
In addition, we have improved the CRY2/CIB1-based light-inducible transcription with split construct optimization.
CRY2/CIB1-based light-inducible transcription was improved by split construct optimization in mammalian cells.
In addition, we have improved the CRY2/CIB1-based light-inducible transcription with split construct optimization.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Approval Evidence
1 source2 linked approval claimsfirst-pass slug fkf1-gigantea-light-inducible-transcription-system
we report newly optimized optogenetic tools to induce transcription with light in mammalian cells, using the Arabidopsis photoreceptor Flavin Kelch-repeat F-box 1 (FKF1) and its binding partner GIGANTEA (GI) ... By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system
Source:
application scopesupports
The optimized FKF1/GI- and CRY2/CIB1-based systems are presented as widely applicable for light-dependent control of transcription in mammalian cells.
The improvements regarding the FKF1/GI- and CRY2/CIB1-based systems will be widely applicable for the light-dependent control of transcription in mammalian cells.
Source:
tool optimizationsupports
Optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells.
By combining the mutagenesis of FKF1 with the optimization of a split FKF1/GI dimerized Gal4-VP16 transcriptional system, we identified constructs enabling significantly improved light-triggered transcriptional induction.
Source:
Comparisons
Source-backed strengths
The source reports that optimized FKF1/GI constructs enabled significantly improved light-triggered transcriptional induction in mammalian cells. The system is implemented as a split FKF1/GI dimerized Gal4-VP16 transcriptional design, indicating a modular architecture for inducible transcriptional activation.
Compared with CRY2-CIB1 light-inducible transcription system
FKF1/GIGANTEA light-inducible transcription system and CRY2-CIB1 light-inducible transcription system address a similar problem space because they share transcription.
Shared frame: same top-level item type; shared target processes: transcription; shared mechanisms: light-induced heterodimerization; same primary input modality: light
Compared with LITEs (Light-inducible transcriptional effectors)
FKF1/GIGANTEA light-inducible transcription system and LITEs (Light-inducible transcriptional effectors) address a similar problem space because they share transcription.
Shared frame: same top-level item type; shared target processes: transcription; shared mechanisms: heterodimerization; same primary input modality: light
Compared with mOptoT7
FKF1/GIGANTEA light-inducible transcription system and mOptoT7 address a similar problem space because they share transcription.
Shared frame: same top-level item type; shared target processes: transcription; shared mechanisms: light-induced heterodimerization; same primary input modality: light
Relative tradeoffs: appears more independently replicated; looks easier to implement in practice.
Ranked Citations
- 1.