Source 1review2014Journal of Cell Science
Toolkit/miniSOG
miniSOG
Taxonomy: Mechanism Branch / Component. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
miniSOG is a genetically encoded protein photosensitizer described as a mini singlet oxygen generator. In the cited AR4-2J cell study, plasma-membrane-targeted miniSOG generated singlet oxygen upon light irradiation and produced photodynamic activation of cholecystokinin 1 receptor (CCK1R), leading to persistent calcium oscillations.
Usefulness & Problems
Why this is useful
miniSOG is useful as a genetically encoded light-responsive source of singlet oxygen for probing photodynamic receptor activation in living cells. The cited work supports its use at the plasma membrane to trigger sustained CCK1R-dependent calcium signaling after illumination.
Source:
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
Problem solved
miniSOG helps solve the problem of producing localized, genetically specified photodynamic activation of CCK1R without relying only on exogenous chemical photosensitizers such as SALPC. The available evidence is limited to this receptor-activation context in AR4-2J cells.
Source:
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
Published Workflows
Objective: Use hybrid QM/MM analysis of natural and engineered LOV domains to understand how intradomain electrostatics control flavin photophysics and to guide future engineering efforts.
Why it works: The workflow compares natural LOV1/LOV2 domains and engineered variants using a common QM/MM framework to connect protein electrostatics and conformational flexibility to excited-state energetics and photophysical outcomes.
electrostatic tuning of the singlet-triplet energy gapcontrol of flavin excited-state energeticscontrol of intersystem crossing efficiencyhybrid QM/MM modelinganalysis of conformational flexibilityanalysis of low-lying singlet and triplet statesprotein electrostatic projection mapping
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Component: A low-level protein part used inside a larger architecture that realizes a mechanism.
Mechanisms
chromophore-assisted laser inactivationlight-triggered singlet oxygen generationphotodynamic receptor activationreactive oxygen species generationTechniques
Selection / EnrichmentTarget processes
selectionInput: Light
Implementation Constraints
The available evidence indicates that miniSOG was genetically encoded and expressed with plasma membrane targeting in AR4-2J cells. Light irradiation was required for activity, but the supplied evidence does not specify excitation parameters, cofactors, or sequence-level construct design.
The supplied evidence supports miniSOG only in a narrow application: photodynamic activation of CCK1R in AR4-2J cells. No quantitative performance metrics, illumination wavelengths, construct architecture details, or independent replication are provided in the supplied evidence.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2review2014Redox Biology
Source 3primary paper2020Biomolecules
Source 4primary paper2026Journal of the American Chemical Society
Ranked Claims
SOPP3 has a smaller energy gap between S1π,π* and TnN,π* than miniSOG and the natural LOV domains analyzed, explaining its improved ability to sensitize triplet oxygen.
SOPP3 was found to have a smaller energy gap between the S1π,π* and TnN,π* compared to miniSOG and all other natural LOV domains, which explains its improved ability to sensitize triplet oxygen.
SOPP3 has a smaller energy gap between S1π,π* and TnN,π* than miniSOG and the natural LOV domains analyzed, explaining its improved ability to sensitize triplet oxygen.
SOPP3 was found to have a smaller energy gap between the S1π,π* and TnN,π* compared to miniSOG and all other natural LOV domains, which explains its improved ability to sensitize triplet oxygen.
SOPP3 has a smaller energy gap between S1π,π* and TnN,π* than miniSOG and the natural LOV domains analyzed, explaining its improved ability to sensitize triplet oxygen.
SOPP3 was found to have a smaller energy gap between the S1π,π* and TnN,π* compared to miniSOG and all other natural LOV domains, which explains its improved ability to sensitize triplet oxygen.
SOPP3 has a smaller energy gap between S1π,π* and TnN,π* than miniSOG and the natural LOV domains analyzed, explaining its improved ability to sensitize triplet oxygen.
SOPP3 was found to have a smaller energy gap between the S1π,π* and TnN,π* compared to miniSOG and all other natural LOV domains, which explains its improved ability to sensitize triplet oxygen.
SOPP3 has a smaller energy gap between S1π,π* and TnN,π* than miniSOG and the natural LOV domains analyzed, explaining its improved ability to sensitize triplet oxygen.
SOPP3 was found to have a smaller energy gap between the S1π,π* and TnN,π* compared to miniSOG and all other natural LOV domains, which explains its improved ability to sensitize triplet oxygen.
A heavy-atom effect alone cannot explain efficient intersystem crossing in LOV domains, especially in Cys-devoid systems like SOPP3.
The results also indicate that a heavy-atom effect alone cannot explain efficient ISC, especially in Cys-devoid systems like SOPP3.
A heavy-atom effect alone cannot explain efficient intersystem crossing in LOV domains, especially in Cys-devoid systems like SOPP3.
The results also indicate that a heavy-atom effect alone cannot explain efficient ISC, especially in Cys-devoid systems like SOPP3.
A heavy-atom effect alone cannot explain efficient intersystem crossing in LOV domains, especially in Cys-devoid systems like SOPP3.
The results also indicate that a heavy-atom effect alone cannot explain efficient ISC, especially in Cys-devoid systems like SOPP3.
A heavy-atom effect alone cannot explain efficient intersystem crossing in LOV domains, especially in Cys-devoid systems like SOPP3.
The results also indicate that a heavy-atom effect alone cannot explain efficient ISC, especially in Cys-devoid systems like SOPP3.
A heavy-atom effect alone cannot explain efficient intersystem crossing in LOV domains, especially in Cys-devoid systems like SOPP3.
The results also indicate that a heavy-atom effect alone cannot explain efficient ISC, especially in Cys-devoid systems like SOPP3.
Protein electrostatics tune the singlet-triplet energy gap in natural and engineered LOV domains.
Together, these results emphasize the importance of electrostatic tuning in controlling the efficiency of ISC in LOV domains.
Protein electrostatics tune the singlet-triplet energy gap in natural and engineered LOV domains.
Together, these results emphasize the importance of electrostatic tuning in controlling the efficiency of ISC in LOV domains.
Protein electrostatics tune the singlet-triplet energy gap in natural and engineered LOV domains.
Together, these results emphasize the importance of electrostatic tuning in controlling the efficiency of ISC in LOV domains.
Protein electrostatics tune the singlet-triplet energy gap in natural and engineered LOV domains.
Together, these results emphasize the importance of electrostatic tuning in controlling the efficiency of ISC in LOV domains.
Protein electrostatics tune the singlet-triplet energy gap in natural and engineered LOV domains.
Together, these results emphasize the importance of electrostatic tuning in controlling the efficiency of ISC in LOV domains.
CCK1R is activated by singlet oxygen generated in photodynamic action with SALPC or genetically encoded protein photosensitizers including KillerRed and miniSOG.
Cholecystokinin 1 receptor (CCK1R) is activated by singlet oxygen (1O2) generated in photodynamic action with sulphonated aluminum phthalocyanine (SALPC) or genetically encoded protein photosensitizer (GEPP) KillerRed or mini singlet oxygen generator (miniSOG).
CCK1R is activated by singlet oxygen generated in photodynamic action with SALPC or genetically encoded protein photosensitizers including KillerRed and miniSOG.
Cholecystokinin 1 receptor (CCK1R) is activated by singlet oxygen (1O2) generated in photodynamic action with sulphonated aluminum phthalocyanine (SALPC) or genetically encoded protein photosensitizer (GEPP) KillerRed or mini singlet oxygen generator (miniSOG).
CCK1R is activated by singlet oxygen generated in photodynamic action with SALPC or genetically encoded protein photosensitizers including KillerRed and miniSOG.
Cholecystokinin 1 receptor (CCK1R) is activated by singlet oxygen (1O2) generated in photodynamic action with sulphonated aluminum phthalocyanine (SALPC) or genetically encoded protein photosensitizer (GEPP) KillerRed or mini singlet oxygen generator (miniSOG).
CCK1R is activated by singlet oxygen generated in photodynamic action with SALPC or genetically encoded protein photosensitizers including KillerRed and miniSOG.
Cholecystokinin 1 receptor (CCK1R) is activated by singlet oxygen (1O2) generated in photodynamic action with sulphonated aluminum phthalocyanine (SALPC) or genetically encoded protein photosensitizer (GEPP) KillerRed or mini singlet oxygen generator (miniSOG).
CCK1R is activated by singlet oxygen generated in photodynamic action with SALPC or genetically encoded protein photosensitizers including KillerRed and miniSOG.
Cholecystokinin 1 receptor (CCK1R) is activated by singlet oxygen (1O2) generated in photodynamic action with sulphonated aluminum phthalocyanine (SALPC) or genetically encoded protein photosensitizer (GEPP) KillerRed or mini singlet oxygen generator (miniSOG).
CCK1R is activated by singlet oxygen generated in photodynamic action with SALPC or genetically encoded protein photosensitizers including KillerRed and miniSOG.
Cholecystokinin 1 receptor (CCK1R) is activated by singlet oxygen (1O2) generated in photodynamic action with sulphonated aluminum phthalocyanine (SALPC) or genetically encoded protein photosensitizer (GEPP) KillerRed or mini singlet oxygen generator (miniSOG).
CCK1R is activated by singlet oxygen generated in photodynamic action with SALPC or genetically encoded protein photosensitizers including KillerRed and miniSOG.
Cholecystokinin 1 receptor (CCK1R) is activated by singlet oxygen (1O2) generated in photodynamic action with sulphonated aluminum phthalocyanine (SALPC) or genetically encoded protein photosensitizer (GEPP) KillerRed or mini singlet oxygen generator (miniSOG).
KillerRed, miniSOG, miniSOG2, SOPP, Mr4511C71G, and DsFbFP expressed at the plasma membrane in AR4-2J cells all triggered persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation.
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
KillerRed, miniSOG, miniSOG2, SOPP, Mr4511C71G, and DsFbFP expressed at the plasma membrane in AR4-2J cells all triggered persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation.
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
KillerRed, miniSOG, miniSOG2, SOPP, Mr4511C71G, and DsFbFP expressed at the plasma membrane in AR4-2J cells all triggered persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation.
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
KillerRed, miniSOG, miniSOG2, SOPP, Mr4511C71G, and DsFbFP expressed at the plasma membrane in AR4-2J cells all triggered persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation.
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
KillerRed, miniSOG, miniSOG2, SOPP, Mr4511C71G, and DsFbFP expressed at the plasma membrane in AR4-2J cells all triggered persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation.
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
KillerRed, miniSOG, miniSOG2, SOPP, Mr4511C71G, and DsFbFP expressed at the plasma membrane in AR4-2J cells all triggered persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation.
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
KillerRed, miniSOG, miniSOG2, SOPP, Mr4511C71G, and DsFbFP expressed at the plasma membrane in AR4-2J cells all triggered persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation.
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
DsFbFP was the least effective among the tested plasma-membrane-targeted genetically encoded photosensitizers because of poor expression.
DsFbFP was the least effective, due to poor expression.
DsFbFP was the least effective among the tested plasma-membrane-targeted genetically encoded photosensitizers because of poor expression.
DsFbFP was the least effective, due to poor expression.
DsFbFP was the least effective among the tested plasma-membrane-targeted genetically encoded photosensitizers because of poor expression.
DsFbFP was the least effective, due to poor expression.
DsFbFP was the least effective among the tested plasma-membrane-targeted genetically encoded photosensitizers because of poor expression.
DsFbFP was the least effective, due to poor expression.
DsFbFP was the least effective among the tested plasma-membrane-targeted genetically encoded photosensitizers because of poor expression.
DsFbFP was the least effective, due to poor expression.
DsFbFP was the least effective among the tested plasma-membrane-targeted genetically encoded photosensitizers because of poor expression.
DsFbFP was the least effective, due to poor expression.
DsFbFP was the least effective among the tested plasma-membrane-targeted genetically encoded photosensitizers because of poor expression.
DsFbFP was the least effective, due to poor expression.
Different plasma-membrane-targeted genetically encoded protein photosensitizers could all photodynamically activate CCK1R.
In conclusion, different GEPPPM could all photodynamically activate CCK1R.
Different plasma-membrane-targeted genetically encoded protein photosensitizers could all photodynamically activate CCK1R.
In conclusion, different GEPPPM could all photodynamically activate CCK1R.
Different plasma-membrane-targeted genetically encoded protein photosensitizers could all photodynamically activate CCK1R.
In conclusion, different GEPPPM could all photodynamically activate CCK1R.
Different plasma-membrane-targeted genetically encoded protein photosensitizers could all photodynamically activate CCK1R.
In conclusion, different GEPPPM could all photodynamically activate CCK1R.
Different plasma-membrane-targeted genetically encoded protein photosensitizers could all photodynamically activate CCK1R.
In conclusion, different GEPPPM could all photodynamically activate CCK1R.
Different plasma-membrane-targeted genetically encoded protein photosensitizers could all photodynamically activate CCK1R.
In conclusion, different GEPPPM could all photodynamically activate CCK1R.
Different plasma-membrane-targeted genetically encoded protein photosensitizers could all photodynamically activate CCK1R.
In conclusion, different GEPPPM could all photodynamically activate CCK1R.
Devazepide at 2 nM readily inhibited LED-induced calcium oscillations in miniSOG plasma-membrane-targeted AR4-2J cells, was less effective in mitochondria-targeted miniSOG cells, and did not inhibit lysosome-targeted miniSOG cells.
In miniSOGPM-AR4-2J cells, light emitting diode (LED) light irradiation-induced calcium oscillations were readily inhibited by CCK1R antagonist devazepide 2 nM; miniSOGMT-AR4-2J cells were less susceptible, but miniSOGLS-AR4-2J cells were not inhibited.
devazepide concentration 2 nM
Devazepide at 2 nM readily inhibited LED-induced calcium oscillations in miniSOG plasma-membrane-targeted AR4-2J cells, was less effective in mitochondria-targeted miniSOG cells, and did not inhibit lysosome-targeted miniSOG cells.
In miniSOGPM-AR4-2J cells, light emitting diode (LED) light irradiation-induced calcium oscillations were readily inhibited by CCK1R antagonist devazepide 2 nM; miniSOGMT-AR4-2J cells were less susceptible, but miniSOGLS-AR4-2J cells were not inhibited.
devazepide concentration 2 nM
Devazepide at 2 nM readily inhibited LED-induced calcium oscillations in miniSOG plasma-membrane-targeted AR4-2J cells, was less effective in mitochondria-targeted miniSOG cells, and did not inhibit lysosome-targeted miniSOG cells.
In miniSOGPM-AR4-2J cells, light emitting diode (LED) light irradiation-induced calcium oscillations were readily inhibited by CCK1R antagonist devazepide 2 nM; miniSOGMT-AR4-2J cells were less susceptible, but miniSOGLS-AR4-2J cells were not inhibited.
devazepide concentration 2 nM
Devazepide at 2 nM readily inhibited LED-induced calcium oscillations in miniSOG plasma-membrane-targeted AR4-2J cells, was less effective in mitochondria-targeted miniSOG cells, and did not inhibit lysosome-targeted miniSOG cells.
In miniSOGPM-AR4-2J cells, light emitting diode (LED) light irradiation-induced calcium oscillations were readily inhibited by CCK1R antagonist devazepide 2 nM; miniSOGMT-AR4-2J cells were less susceptible, but miniSOGLS-AR4-2J cells were not inhibited.
devazepide concentration 2 nM
Devazepide at 2 nM readily inhibited LED-induced calcium oscillations in miniSOG plasma-membrane-targeted AR4-2J cells, was less effective in mitochondria-targeted miniSOG cells, and did not inhibit lysosome-targeted miniSOG cells.
In miniSOGPM-AR4-2J cells, light emitting diode (LED) light irradiation-induced calcium oscillations were readily inhibited by CCK1R antagonist devazepide 2 nM; miniSOGMT-AR4-2J cells were less susceptible, but miniSOGLS-AR4-2J cells were not inhibited.
devazepide concentration 2 nM
Devazepide at 2 nM readily inhibited LED-induced calcium oscillations in miniSOG plasma-membrane-targeted AR4-2J cells, was less effective in mitochondria-targeted miniSOG cells, and did not inhibit lysosome-targeted miniSOG cells.
In miniSOGPM-AR4-2J cells, light emitting diode (LED) light irradiation-induced calcium oscillations were readily inhibited by CCK1R antagonist devazepide 2 nM; miniSOGMT-AR4-2J cells were less susceptible, but miniSOGLS-AR4-2J cells were not inhibited.
devazepide concentration 2 nM
Devazepide at 2 nM readily inhibited LED-induced calcium oscillations in miniSOG plasma-membrane-targeted AR4-2J cells, was less effective in mitochondria-targeted miniSOG cells, and did not inhibit lysosome-targeted miniSOG cells.
In miniSOGPM-AR4-2J cells, light emitting diode (LED) light irradiation-induced calcium oscillations were readily inhibited by CCK1R antagonist devazepide 2 nM; miniSOGMT-AR4-2J cells were less susceptible, but miniSOGLS-AR4-2J cells were not inhibited.
devazepide concentration 2 nM
miniSOG targeted to the plasma membrane, mitochondria, or lysosomes in AR4-2J cells induced persistent calcium oscillations after LED light irradiation.
miniSOG was targeted to PM, mitochondria (MT) or lysosomes (LS) in AR4-2J in parallel experiments; LED light irradiation was found to all induce persistent calcium oscillations.
miniSOG targeted to the plasma membrane, mitochondria, or lysosomes in AR4-2J cells induced persistent calcium oscillations after LED light irradiation.
miniSOG was targeted to PM, mitochondria (MT) or lysosomes (LS) in AR4-2J in parallel experiments; LED light irradiation was found to all induce persistent calcium oscillations.
miniSOG targeted to the plasma membrane, mitochondria, or lysosomes in AR4-2J cells induced persistent calcium oscillations after LED light irradiation.
miniSOG was targeted to PM, mitochondria (MT) or lysosomes (LS) in AR4-2J in parallel experiments; LED light irradiation was found to all induce persistent calcium oscillations.
miniSOG targeted to the plasma membrane, mitochondria, or lysosomes in AR4-2J cells induced persistent calcium oscillations after LED light irradiation.
miniSOG was targeted to PM, mitochondria (MT) or lysosomes (LS) in AR4-2J in parallel experiments; LED light irradiation was found to all induce persistent calcium oscillations.
miniSOG targeted to the plasma membrane, mitochondria, or lysosomes in AR4-2J cells induced persistent calcium oscillations after LED light irradiation.
miniSOG was targeted to PM, mitochondria (MT) or lysosomes (LS) in AR4-2J in parallel experiments; LED light irradiation was found to all induce persistent calcium oscillations.
miniSOG targeted to the plasma membrane, mitochondria, or lysosomes in AR4-2J cells induced persistent calcium oscillations after LED light irradiation.
miniSOG was targeted to PM, mitochondria (MT) or lysosomes (LS) in AR4-2J in parallel experiments; LED light irradiation was found to all induce persistent calcium oscillations.
miniSOG targeted to the plasma membrane, mitochondria, or lysosomes in AR4-2J cells induced persistent calcium oscillations after LED light irradiation.
miniSOG was targeted to PM, mitochondria (MT) or lysosomes (LS) in AR4-2J in parallel experiments; LED light irradiation was found to all induce persistent calcium oscillations.
miniSOG is associated with correlative light and electron microscopy applications in the supplied source scaffold.
SuperNova and miniSOG are associated with chromophore-assisted light inactivation workflows in the supplied source scaffold.
At the organelle level, including mitochondria, plasma membrane, or lysosomes, CALI can trigger cell death.
CALI can provide information about individual events involved in target protein function and highlight them within multifactorial events.
CALI has emerged as an optogenetic tool to switch off signaling pathways, including optical depletion of individual neurons.
CALI of nuclear proteins can induce cell cycle arrest and chromatin- or locus-specific DNA damage.
Rescue experiments can clarify phenotypic capabilities after CALI depletion of endogenous targets.
Using spatially restricted microscopy illumination, CALI can address protein isoform, subcellular localization, and phase-specific questions that RNA interference or chemical treatment cannot.
CALI is performed using photosensitizers that generate reactive oxygen species.
CALI enables spatiotemporal knockdown or loss-of-function of target molecules in situ.
The review describes two CALI approaches: transgenic tags with chemical photosensitizers and genetically encoded fluorescent protein fusions.
This review centers on genetically encoded ROS-generating proteins for optogenetic control of reactive oxygen species, with KillerRed, miniSOG, and SuperNova highlighted as core examples.
Approval Evidence
4 sources10 linked approval claimsfirst-pass slug minisog
This work focuses on ... two engineered protein variants used for singlet oxygen generation, miniSOG and SOPP3.
Source:
mini singlet oxygen generator (miniSOG)
Source:
Additional high-signal enrichment leads cluster into four useful categories: foundational CALI methodology, mechanistic papers explaining ROS-mediated inactivation, genetically encoded photosensitizer/tool-development papers (notably KillerRed, miniSOG, SuperNova), and representative application papers in neurons, mitochondria, nuclei, and whole-animal cell ablation.
Source:
The anchor review explicitly centers on genetically encoded ROS-generating proteins used for optogenetic control of reactive oxygen species, especially KillerRed, miniSOG, and the then-new monomeric derivative SuperNova.
Source:
comparative propertysupports
SOPP3 has a smaller energy gap between S1π,π* and TnN,π* than miniSOG and the natural LOV domains analyzed, explaining its improved ability to sensitize triplet oxygen.
SOPP3 was found to have a smaller energy gap between the S1π,π* and TnN,π* compared to miniSOG and all other natural LOV domains, which explains its improved ability to sensitize triplet oxygen.
Source:
mechanistic insightsupports
Protein electrostatics tune the singlet-triplet energy gap in natural and engineered LOV domains.
Together, these results emphasize the importance of electrostatic tuning in controlling the efficiency of ISC in LOV domains.
Source:
activationsupports
CCK1R is activated by singlet oxygen generated in photodynamic action with SALPC or genetically encoded protein photosensitizers including KillerRed and miniSOG.
Cholecystokinin 1 receptor (CCK1R) is activated by singlet oxygen (1O2) generated in photodynamic action with sulphonated aluminum phthalocyanine (SALPC) or genetically encoded protein photosensitizer (GEPP) KillerRed or mini singlet oxygen generator (miniSOG).
Source:
application resultsupports
KillerRed, miniSOG, miniSOG2, SOPP, Mr4511C71G, and DsFbFP expressed at the plasma membrane in AR4-2J cells all triggered persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation.
KillerRed, miniSOG, miniSOG2, singlet oxygen protein photosensitizer (SOPP), flavin-binding fluorescent protein from Methylobacterium radiotolerans with point mutation C71G (Mr4511C71G), and flavin-binding fluorescent protein from Dinoroseobacter shibae (DsFbFP) were expressed at the plasma membrane (PM) in AR4-2J cells, which express endogenous CCK1R. Light irradiation ... of GEPPPM-expressing AR4-2J was found to all trigger persistent calcium oscillations, a hallmark of permanent photodynamic CCK1R activation; DsFbFP was the least effective, due to poor expression.
Source:
conclusionsupports
Different plasma-membrane-targeted genetically encoded protein photosensitizers could all photodynamically activate CCK1R.
In conclusion, different GEPPPM could all photodynamically activate CCK1R.
Source:
pharmacological modulationsupports
Devazepide at 2 nM readily inhibited LED-induced calcium oscillations in miniSOG plasma-membrane-targeted AR4-2J cells, was less effective in mitochondria-targeted miniSOG cells, and did not inhibit lysosome-targeted miniSOG cells.
In miniSOGPM-AR4-2J cells, light emitting diode (LED) light irradiation-induced calcium oscillations were readily inhibited by CCK1R antagonist devazepide 2 nM; miniSOGMT-AR4-2J cells were less susceptible, but miniSOGLS-AR4-2J cells were not inhibited.
Source:
subcellular targeting resultsupports
miniSOG targeted to the plasma membrane, mitochondria, or lysosomes in AR4-2J cells induced persistent calcium oscillations after LED light irradiation.
miniSOG was targeted to PM, mitochondria (MT) or lysosomes (LS) in AR4-2J in parallel experiments; LED light irradiation was found to all induce persistent calcium oscillations.
Source:
application associationsupports
miniSOG is associated with correlative light and electron microscopy applications in the supplied source scaffold.
Source:
application associationsupports
SuperNova and miniSOG are associated with chromophore-assisted light inactivation workflows in the supplied source scaffold.
Source:
review scope summarysupports
This review centers on genetically encoded ROS-generating proteins for optogenetic control of reactive oxygen species, with KillerRed, miniSOG, and SuperNova highlighted as core examples.
Source:
Comparisons
Source-backed strengths
The cited study shows that plasma-membrane-targeted miniSOG was effective in triggering persistent calcium oscillations upon light irradiation, consistent with permanent photodynamic CCK1R activation. miniSOG was grouped with other effective genetically encoded photosensitizers, and the only explicitly identified poor performer was DsFbFP due to poor expression.
Source:
DsFbFP was the least effective, due to poor expression.
Ranked Citations
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