Toolkit/H2O2-responsive promoter-driven nuclear-encoded reporter gene
H2O2-responsive promoter-driven nuclear-encoded reporter gene
Also known as: nuclear-encoded reporter gene driven by this promoter, promoter that specifically responded to H2O2
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
This tool is a nuclear-encoded reporter construct in Chlamydomonas reinhardtii driven by a promoter reported to respond specifically to H2O2. It is used to monitor H2O2-dependent transcriptional signaling, with reporter induction influenced by exogenous H2O2 and by light-dependent photosynthetic physiology.
Usefulness & Problems
Why this is useful
The construct provides a genetically encoded readout for H2O2-responsive signaling in C. reinhardtii. It is useful for probing how light and photosynthetic electron flow alter cellular H2O2 signaling output through effects on catalase activity and H2O2 accumulation.
Problem solved
This tool addresses the problem of detecting a specific H2O2 signaling response in vivo rather than inferring reactive oxygen species effects indirectly. The cited work indicates that it enables assessment of how exogenous H2O2 and illumination state modulate transcriptional output in algal cells.
Problem links
Need conditional control of signaling activity
DerivedThis tool is a nuclear-encoded reporter construct in Chlamydomonas reinhardtii driven by a promoter reported to respond specifically to H2O2. It is used to monitor H2O2-dependent transcriptional signaling, with reporter induction influenced by exogenous H2O2 and by light-dependent photosynthetic physiology.
Need conditional recombination or state switching
DerivedThis tool is a nuclear-encoded reporter construct in Chlamydomonas reinhardtii driven by a promoter reported to respond specifically to H2O2. It is used to monitor H2O2-dependent transcriptional signaling, with reporter induction influenced by exogenous H2O2 and by light-dependent photosynthetic physiology.
Need precise spatiotemporal control with light input
DerivedThis tool is a nuclear-encoded reporter construct in Chlamydomonas reinhardtii driven by a promoter reported to respond specifically to H2O2. It is used to monitor H2O2-dependent transcriptional signaling, with reporter induction influenced by exogenous H2O2 and by light-dependent photosynthetic physiology.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Mechanisms
h2o2-responsive transcriptional activationlight-dependent modulation of reporter inductionphotosynthetic electron transport-dependent down-regulation of catalase activityphotosynthetic electron transport-dependent regulation of catalase activityTechniques
No technique tags yet.
Target processes
recombinationsignalingInput: Light
Implementation Constraints
The construct is described as a nuclear-encoded reporter gene driven by an H2O2-responsive promoter in C. reinhardtii. Practical use appears to require control of exogenous H2O2 and illumination conditions, and interpretation is affected by photosynthetic electron transport because DCMU prevented the light-controlled down-regulation of catalase activity.
The available evidence is limited to a single cited study in C. reinhardtii and does not provide broader cross-species validation or extensive construct performance metrics. The exact promoter identity, reporter gene identity, dynamic range, kinetics, and baseline expression characteristics are not provided in the supplied evidence.
Validation
Supporting Sources
Ranked Claims
Induction of the H2O2-responsive reporter gene depends on both exogenously added H2O2 level and light, with lower induction in the dark than in the light.
Expression of a nuclear-encoded reporter gene driven by this promoter was shown to depend not only on the level of exogenously added H(2)O(2) but also on light. In the dark, the induction of the reporter gene by H(2)O(2) was much lower than in the light.
Induction of the H2O2-responsive reporter gene depends on both exogenously added H2O2 level and light, with lower induction in the dark than in the light.
Expression of a nuclear-encoded reporter gene driven by this promoter was shown to depend not only on the level of exogenously added H(2)O(2) but also on light. In the dark, the induction of the reporter gene by H(2)O(2) was much lower than in the light.
Induction of the H2O2-responsive reporter gene depends on both exogenously added H2O2 level and light, with lower induction in the dark than in the light.
Expression of a nuclear-encoded reporter gene driven by this promoter was shown to depend not only on the level of exogenously added H(2)O(2) but also on light. In the dark, the induction of the reporter gene by H(2)O(2) was much lower than in the light.
Induction of the H2O2-responsive reporter gene depends on both exogenously added H2O2 level and light, with lower induction in the dark than in the light.
Expression of a nuclear-encoded reporter gene driven by this promoter was shown to depend not only on the level of exogenously added H(2)O(2) but also on light. In the dark, the induction of the reporter gene by H(2)O(2) was much lower than in the light.
Induction of the H2O2-responsive reporter gene depends on both exogenously added H2O2 level and light, with lower induction in the dark than in the light.
Expression of a nuclear-encoded reporter gene driven by this promoter was shown to depend not only on the level of exogenously added H(2)O(2) but also on light. In the dark, the induction of the reporter gene by H(2)O(2) was much lower than in the light.
Induction of the H2O2-responsive reporter gene depends on both exogenously added H2O2 level and light, with lower induction in the dark than in the light.
Expression of a nuclear-encoded reporter gene driven by this promoter was shown to depend not only on the level of exogenously added H(2)O(2) but also on light. In the dark, the induction of the reporter gene by H(2)O(2) was much lower than in the light.
Induction of the H2O2-responsive reporter gene depends on both exogenously added H2O2 level and light, with lower induction in the dark than in the light.
Expression of a nuclear-encoded reporter gene driven by this promoter was shown to depend not only on the level of exogenously added H(2)O(2) but also on light. In the dark, the induction of the reporter gene by H(2)O(2) was much lower than in the light.
A light-induced reduction in catalase activity keeps H2O2 levels higher in the light.
Due to a light-induced reduction in catalase activity, H(2)O(2) levels in the light remained higher.
A light-induced reduction in catalase activity keeps H2O2 levels higher in the light.
Due to a light-induced reduction in catalase activity, H(2)O(2) levels in the light remained higher.
A light-induced reduction in catalase activity keeps H2O2 levels higher in the light.
Due to a light-induced reduction in catalase activity, H(2)O(2) levels in the light remained higher.
A light-induced reduction in catalase activity keeps H2O2 levels higher in the light.
Due to a light-induced reduction in catalase activity, H(2)O(2) levels in the light remained higher.
A light-induced reduction in catalase activity keeps H2O2 levels higher in the light.
Due to a light-induced reduction in catalase activity, H(2)O(2) levels in the light remained higher.
A light-induced reduction in catalase activity keeps H2O2 levels higher in the light.
Due to a light-induced reduction in catalase activity, H(2)O(2) levels in the light remained higher.
A light-induced reduction in catalase activity keeps H2O2 levels higher in the light.
Due to a light-induced reduction in catalase activity, H(2)O(2) levels in the light remained higher.
Photosynthetic electron transport mediates the light-controlled down-regulation of catalase activity because DCMU prevents this down-regulation.
Photosynthetic electron transport mediated the light-controlled down-regulation of the catalase activity since it was prevented by 3-(3'4'-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosystem II.
Photosynthetic electron transport mediates the light-controlled down-regulation of catalase activity because DCMU prevents this down-regulation.
Photosynthetic electron transport mediated the light-controlled down-regulation of the catalase activity since it was prevented by 3-(3'4'-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosystem II.
Photosynthetic electron transport mediates the light-controlled down-regulation of catalase activity because DCMU prevents this down-regulation.
Photosynthetic electron transport mediated the light-controlled down-regulation of the catalase activity since it was prevented by 3-(3'4'-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosystem II.
Photosynthetic electron transport mediates the light-controlled down-regulation of catalase activity because DCMU prevents this down-regulation.
Photosynthetic electron transport mediated the light-controlled down-regulation of the catalase activity since it was prevented by 3-(3'4'-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosystem II.
Photosynthetic electron transport mediates the light-controlled down-regulation of catalase activity because DCMU prevents this down-regulation.
Photosynthetic electron transport mediated the light-controlled down-regulation of the catalase activity since it was prevented by 3-(3'4'-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosystem II.
Photosynthetic electron transport mediates the light-controlled down-regulation of catalase activity because DCMU prevents this down-regulation.
Photosynthetic electron transport mediated the light-controlled down-regulation of the catalase activity since it was prevented by 3-(3'4'-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosystem II.
Photosynthetic electron transport mediates the light-controlled down-regulation of catalase activity because DCMU prevents this down-regulation.
Photosynthetic electron transport mediated the light-controlled down-regulation of the catalase activity since it was prevented by 3-(3'4'-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosystem II.
Lower reporter induction in the dark correlates with faster disappearance of H2O2 from the culture medium in the dark.
This lower induction was correlated with an accelerated disappearance of H(2)O(2) from the culture medium in the dark.
Lower reporter induction in the dark correlates with faster disappearance of H2O2 from the culture medium in the dark.
This lower induction was correlated with an accelerated disappearance of H(2)O(2) from the culture medium in the dark.
Lower reporter induction in the dark correlates with faster disappearance of H2O2 from the culture medium in the dark.
This lower induction was correlated with an accelerated disappearance of H(2)O(2) from the culture medium in the dark.
Lower reporter induction in the dark correlates with faster disappearance of H2O2 from the culture medium in the dark.
This lower induction was correlated with an accelerated disappearance of H(2)O(2) from the culture medium in the dark.
Lower reporter induction in the dark correlates with faster disappearance of H2O2 from the culture medium in the dark.
This lower induction was correlated with an accelerated disappearance of H(2)O(2) from the culture medium in the dark.
Lower reporter induction in the dark correlates with faster disappearance of H2O2 from the culture medium in the dark.
This lower induction was correlated with an accelerated disappearance of H(2)O(2) from the culture medium in the dark.
Lower reporter induction in the dark correlates with faster disappearance of H2O2 from the culture medium in the dark.
This lower induction was correlated with an accelerated disappearance of H(2)O(2) from the culture medium in the dark.
In light plus DCMU, reporter expression is low, whereas aminotriazole increases H2O2-induced reporter expression in the dark.
In the presence of light and DCMU, expression of the reporter gene was low while the addition of aminotriazole, a catalase inhibitor, led to a higher induction of the reporter gene by H(2)O(2) in the dark.
In light plus DCMU, reporter expression is low, whereas aminotriazole increases H2O2-induced reporter expression in the dark.
In the presence of light and DCMU, expression of the reporter gene was low while the addition of aminotriazole, a catalase inhibitor, led to a higher induction of the reporter gene by H(2)O(2) in the dark.
In light plus DCMU, reporter expression is low, whereas aminotriazole increases H2O2-induced reporter expression in the dark.
In the presence of light and DCMU, expression of the reporter gene was low while the addition of aminotriazole, a catalase inhibitor, led to a higher induction of the reporter gene by H(2)O(2) in the dark.
In light plus DCMU, reporter expression is low, whereas aminotriazole increases H2O2-induced reporter expression in the dark.
In the presence of light and DCMU, expression of the reporter gene was low while the addition of aminotriazole, a catalase inhibitor, led to a higher induction of the reporter gene by H(2)O(2) in the dark.
In light plus DCMU, reporter expression is low, whereas aminotriazole increases H2O2-induced reporter expression in the dark.
In the presence of light and DCMU, expression of the reporter gene was low while the addition of aminotriazole, a catalase inhibitor, led to a higher induction of the reporter gene by H(2)O(2) in the dark.
In light plus DCMU, reporter expression is low, whereas aminotriazole increases H2O2-induced reporter expression in the dark.
In the presence of light and DCMU, expression of the reporter gene was low while the addition of aminotriazole, a catalase inhibitor, led to a higher induction of the reporter gene by H(2)O(2) in the dark.
In light plus DCMU, reporter expression is low, whereas aminotriazole increases H2O2-induced reporter expression in the dark.
In the presence of light and DCMU, expression of the reporter gene was low while the addition of aminotriazole, a catalase inhibitor, led to a higher induction of the reporter gene by H(2)O(2) in the dark.
The authors propose that a controlled down-regulation of catalase activity after a dark-to-light shift is necessary to maintain H2O2 at a level required for activation of H2O2-dependent signaling pathways.
It is proposed that, contrary to expectations, a controlled down-regulation of catalase activity occurs upon a shift of cells from dark to light. This down-regulation apparently is necessary to maintain a certain level of H(2)O(2) required to activate H(2)O(2)-dependent signaling pathways.
The authors propose that a controlled down-regulation of catalase activity after a dark-to-light shift is necessary to maintain H2O2 at a level required for activation of H2O2-dependent signaling pathways.
It is proposed that, contrary to expectations, a controlled down-regulation of catalase activity occurs upon a shift of cells from dark to light. This down-regulation apparently is necessary to maintain a certain level of H(2)O(2) required to activate H(2)O(2)-dependent signaling pathways.
The authors propose that a controlled down-regulation of catalase activity after a dark-to-light shift is necessary to maintain H2O2 at a level required for activation of H2O2-dependent signaling pathways.
It is proposed that, contrary to expectations, a controlled down-regulation of catalase activity occurs upon a shift of cells from dark to light. This down-regulation apparently is necessary to maintain a certain level of H(2)O(2) required to activate H(2)O(2)-dependent signaling pathways.
The authors propose that a controlled down-regulation of catalase activity after a dark-to-light shift is necessary to maintain H2O2 at a level required for activation of H2O2-dependent signaling pathways.
It is proposed that, contrary to expectations, a controlled down-regulation of catalase activity occurs upon a shift of cells from dark to light. This down-regulation apparently is necessary to maintain a certain level of H(2)O(2) required to activate H(2)O(2)-dependent signaling pathways.
The authors propose that a controlled down-regulation of catalase activity after a dark-to-light shift is necessary to maintain H2O2 at a level required for activation of H2O2-dependent signaling pathways.
It is proposed that, contrary to expectations, a controlled down-regulation of catalase activity occurs upon a shift of cells from dark to light. This down-regulation apparently is necessary to maintain a certain level of H(2)O(2) required to activate H(2)O(2)-dependent signaling pathways.
The authors propose that a controlled down-regulation of catalase activity after a dark-to-light shift is necessary to maintain H2O2 at a level required for activation of H2O2-dependent signaling pathways.
It is proposed that, contrary to expectations, a controlled down-regulation of catalase activity occurs upon a shift of cells from dark to light. This down-regulation apparently is necessary to maintain a certain level of H(2)O(2) required to activate H(2)O(2)-dependent signaling pathways.
The authors propose that a controlled down-regulation of catalase activity after a dark-to-light shift is necessary to maintain H2O2 at a level required for activation of H2O2-dependent signaling pathways.
It is proposed that, contrary to expectations, a controlled down-regulation of catalase activity occurs upon a shift of cells from dark to light. This down-regulation apparently is necessary to maintain a certain level of H(2)O(2) required to activate H(2)O(2)-dependent signaling pathways.
The paper defines a promoter in Chlamydomonas reinhardtii that specifically responds to H2O2 and can drive a nuclear-encoded reporter gene.
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
The paper defines a promoter in Chlamydomonas reinhardtii that specifically responds to H2O2 and can drive a nuclear-encoded reporter gene.
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
The paper defines a promoter in Chlamydomonas reinhardtii that specifically responds to H2O2 and can drive a nuclear-encoded reporter gene.
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
The paper defines a promoter in Chlamydomonas reinhardtii that specifically responds to H2O2 and can drive a nuclear-encoded reporter gene.
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
The paper defines a promoter in Chlamydomonas reinhardtii that specifically responds to H2O2 and can drive a nuclear-encoded reporter gene.
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
The paper defines a promoter in Chlamydomonas reinhardtii that specifically responds to H2O2 and can drive a nuclear-encoded reporter gene.
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
The paper defines a promoter in Chlamydomonas reinhardtii that specifically responds to H2O2 and can drive a nuclear-encoded reporter gene.
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
Approval Evidence
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
Source:
Induction of the H2O2-responsive reporter gene depends on both exogenously added H2O2 level and light, with lower induction in the dark than in the light.
Expression of a nuclear-encoded reporter gene driven by this promoter was shown to depend not only on the level of exogenously added H(2)O(2) but also on light. In the dark, the induction of the reporter gene by H(2)O(2) was much lower than in the light.
Source:
A light-induced reduction in catalase activity keeps H2O2 levels higher in the light.
Due to a light-induced reduction in catalase activity, H(2)O(2) levels in the light remained higher.
Source:
Photosynthetic electron transport mediates the light-controlled down-regulation of catalase activity because DCMU prevents this down-regulation.
Photosynthetic electron transport mediated the light-controlled down-regulation of the catalase activity since it was prevented by 3-(3'4'-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosystem II.
Source:
Lower reporter induction in the dark correlates with faster disappearance of H2O2 from the culture medium in the dark.
This lower induction was correlated with an accelerated disappearance of H(2)O(2) from the culture medium in the dark.
Source:
In light plus DCMU, reporter expression is low, whereas aminotriazole increases H2O2-induced reporter expression in the dark.
In the presence of light and DCMU, expression of the reporter gene was low while the addition of aminotriazole, a catalase inhibitor, led to a higher induction of the reporter gene by H(2)O(2) in the dark.
Source:
The authors propose that a controlled down-regulation of catalase activity after a dark-to-light shift is necessary to maintain H2O2 at a level required for activation of H2O2-dependent signaling pathways.
It is proposed that, contrary to expectations, a controlled down-regulation of catalase activity occurs upon a shift of cells from dark to light. This down-regulation apparently is necessary to maintain a certain level of H(2)O(2) required to activate H(2)O(2)-dependent signaling pathways.
Source:
The paper defines a promoter in Chlamydomonas reinhardtii that specifically responds to H2O2 and can drive a nuclear-encoded reporter gene.
A specific signaling role for H(2)O(2) in Chlamydomonas reinhardtii was demonstrated by the definition of a promoter that specifically responded to this ROS. Expression of a nuclear-encoded reporter gene driven by this promoter...
Source:
Comparisons
Source-backed strengths
The source literature states that the promoter specifically responded to H2O2, supporting specificity at the level of transcriptional activation. Reporter induction was shown to depend on both exogenous H2O2 concentration and light, and the associated study linked this light effect to photosynthetic electron transport and catalase down-regulation.
Compared with cell-type specific Cre-driver mouse lines
H2O2-responsive promoter-driven nuclear-encoded reporter gene and cell-type specific Cre-driver mouse lines address a similar problem space because they share recombination, signaling.
Shared frame: same top-level item type; shared target processes: recombination, signaling; same primary input modality: light
Compared with CfRhPDE1
H2O2-responsive promoter-driven nuclear-encoded reporter gene and CfRhPDE1 address a similar problem space because they share recombination, signaling.
Shared frame: same top-level item type; shared target processes: recombination, signaling; same primary input modality: light
Compared with photobiomodulation therapy
H2O2-responsive promoter-driven nuclear-encoded reporter gene and photobiomodulation therapy address a similar problem space because they share recombination, signaling.
Shared frame: same top-level item type; shared target processes: recombination, signaling; same primary input modality: light
Ranked Citations
- 1.