Toolkit/PiGM-Iq
PiGM-Iq
Also known as: Photo-induced Modulation of Gα protein – Inhibition of Gα q
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
PiGM-Iq is a light-controlled multi-component switch for Photo-induced Modulation of Gα protein signaling that inhibits Gαq. The reported system produced potent and selective inhibition of Gαq signaling and was applied to perturb signaling-dependent neural development and behavior.
Usefulness & Problems
Why this is useful
PiGM-Iq is useful for optically perturbing Gαq-dependent signaling with reported potency and selectivity. It enabled experimental manipulation of neural development and behavior in cultured neurons, zebrafish, C. elegans, and Drosophila.
Source:
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
Source:
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
Source:
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
Source:
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
Problem solved
PiGM-Iq addresses the problem of controlling Gαq signaling with light in order to test causal roles of this pathway in development, circuit formation, and behavior. The supplied evidence specifically supports its use for inhibiting Gαq signaling in vivo and in cultured neurons.
Source:
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
Source:
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
Source:
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
Source:
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
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
localizationsignalingInput: Light
Implementation Constraints
PiGM-Iq is described as a light-controlled multi-component switch and is associated with membrane recruitment and domain fusion. The provided evidence does not specify the photoreceptor components, expression strategy, cofactors, illumination regime, or delivery method.
The supplied evidence does not provide quantitative performance metrics, kinetic parameters, wavelength details, or construct architecture beyond identifying it as a light-controlled multi-component switch. Independent replication is not shown in the provided material, and validation appears to derive from a single 2023 study.
Validation
Supporting Sources
Ranked Claims
PiGM-Iq activation in zebrafish embryos and larvae led to developmental deficits resulting in altered neuronal wiring and behavior.
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
PiGM-Iq activation in zebrafish embryos and larvae led to developmental deficits resulting in altered neuronal wiring and behavior.
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
PiGM-Iq activation in zebrafish embryos and larvae led to developmental deficits resulting in altered neuronal wiring and behavior.
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
PiGM-Iq activation in zebrafish embryos and larvae led to developmental deficits resulting in altered neuronal wiring and behavior.
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
PiGM-Iq activation in zebrafish embryos and larvae led to developmental deficits resulting in altered neuronal wiring and behavior.
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
PiGM-Iq activation in zebrafish embryos and larvae led to developmental deficits resulting in altered neuronal wiring and behavior.
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
PiGM-Iq activation in zebrafish embryos and larvae led to developmental deficits resulting in altered neuronal wiring and behavior.
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
PiGM-Iq altered behavior in C. elegans and Drosophila with outcomes consistent with GPCR-Gαq disruption.
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
PiGM-Iq altered behavior in C. elegans and Drosophila with outcomes consistent with GPCR-Gαq disruption.
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
PiGM-Iq altered behavior in C. elegans and Drosophila with outcomes consistent with GPCR-Gαq disruption.
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
PiGM-Iq altered behavior in C. elegans and Drosophila with outcomes consistent with GPCR-Gαq disruption.
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
PiGM-Iq altered behavior in C. elegans and Drosophila with outcomes consistent with GPCR-Gαq disruption.
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
PiGM-Iq altered behavior in C. elegans and Drosophila with outcomes consistent with GPCR-Gαq disruption.
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
PiGM-Iq altered behavior in C. elegans and Drosophila with outcomes consistent with GPCR-Gαq disruption.
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
PiGM-Iq changed axon guidance in cultured dorsal root ganglion neurons in response to serotonin.
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
PiGM-Iq changed axon guidance in cultured dorsal root ganglion neurons in response to serotonin.
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
PiGM-Iq changed axon guidance in cultured dorsal root ganglion neurons in response to serotonin.
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
PiGM-Iq changed axon guidance in cultured dorsal root ganglion neurons in response to serotonin.
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
PiGM-Iq changed axon guidance in cultured dorsal root ganglion neurons in response to serotonin.
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
PiGM-Iq changed axon guidance in cultured dorsal root ganglion neurons in response to serotonin.
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
PiGM-Iq changed axon guidance in cultured dorsal root ganglion neurons in response to serotonin.
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
PiGM-Iq exhibited potent and selective inhibition of Gαq signaling.
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
PiGM-Iq exhibited potent and selective inhibition of Gαq signaling.
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
PiGM-Iq exhibited potent and selective inhibition of Gαq signaling.
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
PiGM-Iq exhibited potent and selective inhibition of Gαq signaling.
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
PiGM-Iq exhibited potent and selective inhibition of Gαq signaling.
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
PiGM-Iq exhibited potent and selective inhibition of Gαq signaling.
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
PiGM-Iq exhibited potent and selective inhibition of Gαq signaling.
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
By altering the minimal RGS domain, the approach is amenable to Gαi signaling.
By altering the choice of minimal RGS domain, we also show that this approach is amenable to Gα i signaling.
By altering the minimal RGS domain, the approach is amenable to Gαi signaling.
By altering the choice of minimal RGS domain, we also show that this approach is amenable to Gα i signaling.
By altering the minimal RGS domain, the approach is amenable to Gαi signaling.
By altering the choice of minimal RGS domain, we also show that this approach is amenable to Gα i signaling.
By altering the minimal RGS domain, the approach is amenable to Gαi signaling.
By altering the choice of minimal RGS domain, we also show that this approach is amenable to Gα i signaling.
By altering the minimal RGS domain, the approach is amenable to Gαi signaling.
By altering the choice of minimal RGS domain, we also show that this approach is amenable to Gα i signaling.
By altering the minimal RGS domain, the approach is amenable to Gαi signaling.
By altering the choice of minimal RGS domain, we also show that this approach is amenable to Gα i signaling.
By altering the minimal RGS domain, the approach is amenable to Gαi signaling.
By altering the choice of minimal RGS domain, we also show that this approach is amenable to Gα i signaling.
The authors developed and validated an optogenetic tool that disrupts Gαq signaling through membrane recruitment of a minimal RGS domain.
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
The authors developed and validated an optogenetic tool that disrupts Gαq signaling through membrane recruitment of a minimal RGS domain.
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
The authors developed and validated an optogenetic tool that disrupts Gαq signaling through membrane recruitment of a minimal RGS domain.
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
The authors developed and validated an optogenetic tool that disrupts Gαq signaling through membrane recruitment of a minimal RGS domain.
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
The authors developed and validated an optogenetic tool that disrupts Gαq signaling through membrane recruitment of a minimal RGS domain.
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
The authors developed and validated an optogenetic tool that disrupts Gαq signaling through membrane recruitment of a minimal RGS domain.
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
The authors developed and validated an optogenetic tool that disrupts Gαq signaling through membrane recruitment of a minimal RGS domain.
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
Approval Evidence
This approach, Photo-induced Modulation of Gα protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
Source:
PiGM-Iq activation in zebrafish embryos and larvae led to developmental deficits resulting in altered neuronal wiring and behavior.
PiGM-Iq activation leads to developmental deficits in zebrafish embryos and larvae resulting in altered neuronal wiring and behavior.
Source:
PiGM-Iq altered behavior in C. elegans and Drosophila with outcomes consistent with GPCR-Gαq disruption.
We alter the behavior of C. elegans and Drosophila with outcomes consistent with GPCR-Gα q disruption.
Source:
PiGM-Iq changed axon guidance in cultured dorsal root ganglion neurons in response to serotonin.
PiGM-Iq also changes axon guidance in culture dorsal root ganglia neurons in response to serotonin.
Source:
PiGM-Iq exhibited potent and selective inhibition of Gαq signaling.
This approach, Photo-induced Modulation of G α protein – Inhibition of Gα q (PiGM-Iq), exhibited potent and selective inhibition of Gα q signaling.
Source:
By altering the minimal RGS domain, the approach is amenable to Gαi signaling.
By altering the choice of minimal RGS domain, we also show that this approach is amenable to Gα i signaling.
Source:
The authors developed and validated an optogenetic tool that disrupts Gαq signaling through membrane recruitment of a minimal RGS domain.
In this work, we develop and validate a new optogenetic tool that disrupt Gα q signaling through membrane recruitment of a minimal Regulator of G-protein signaling (RGS) domain.
Source:
Comparisons
Source-backed strengths
The source reports potent and selective inhibition of Gαq signaling. Functional effects were observed across multiple biological contexts, including dorsal root ganglion neurons, zebrafish embryos and larvae, C. elegans, and Drosophila, with phenotypes consistent with GPCR-Gαq disruption.
Ranked Citations
- 1.