Toolkit/Set2-LANS optogenetic switch
Set2-LANS optogenetic switch
Also known as: optogenetic control for Set2, Set2-LANS
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Set2-LANS is an optogenetic fusion of the yeast H3K36 methyltransferase Set2 with the light-activated nuclear shuttle (LANS) domain. It provides rapid and reversible light control of Set2, enabling inducible nuclear localization and control of H3K36 methylation in vivo.
Usefulness & Problems
Why this is useful
This tool is useful for temporally controlling the activity of Set2, the sole H3K36 methyltransferase in yeast, with light. The cited study used it to probe dynamics of H3K36 methylation, including relationships between H3K36me3, RNA abundance, and demethylation by Rph1.
Source:
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
Problem solved
Set2-LANS addresses the problem of achieving rapid and reversible control over Set2 function in living yeast cells. This enables perturbation of H3K36 methylation dynamics without relying solely on static genetic manipulations.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A composed arrangement of multiple parts that instantiates one or more mechanisms.
Mechanisms
histone h3k36 trimethylation depositionlight-controlled nuclear localizationreversible subcellular shuttlingTechniques
No technique tags yet.
Target processes
localizationtranscriptionInput: Light
Implementation Constraints
Implementation involved fusing yeast Set2 to the light-activated nuclear shuttle (LANS) domain to create an optogenetic switch. The available evidence supports use in yeast in vivo, but does not provide additional practical details such as promoter choice, expression system, or light-delivery conditions.
The supplied evidence does not specify illumination wavelength, kinetic parameters, dynamic range, or construct architecture beyond Set2-LANS fusion. Independent replication is not provided in the supplied sources, and validation details outside yeast are not described.
Validation
Observations
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Section: abstract. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Section: abstract. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Section: abstract. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Section: abstract. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Section: abstract. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Section: abstract. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Inferred from claim c2 during normalization. Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo. Derived from claim c2. Section: abstract. Quoted text: Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Supporting Sources
Ranked Claims
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
The authors established rapid and reversible optogenetic control of yeast Set2 by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The authors established rapid and reversible optogenetic control of yeast Set2 by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The authors established rapid and reversible optogenetic control of yeast Set2 by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The authors established rapid and reversible optogenetic control of yeast Set2 by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The authors established rapid and reversible optogenetic control of yeast Set2 by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The authors established rapid and reversible optogenetic control of yeast Set2 by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The authors established rapid and reversible optogenetic control of yeast Set2 by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting directed deposition on all transcribed genes regardless of overall transcription frequency.
relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting directed deposition on all transcribed genes regardless of overall transcription frequency.
relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting directed deposition on all transcribed genes regardless of overall transcription frequency.
relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting directed deposition on all transcribed genes regardless of overall transcription frequency.
relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting directed deposition on all transcribed genes regardless of overall transcription frequency.
relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting directed deposition on all transcribed genes regardless of overall transcription frequency.
relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting directed deposition on all transcribed genes regardless of overall transcription frequency.
relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting that H3K36 demethylases act in a global, stochastic manner.
the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting that H3K36 demethylases act in a global, stochastic manner.
the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting that H3K36 demethylases act in a global, stochastic manner.
the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting that H3K36 demethylases act in a global, stochastic manner.
the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting that H3K36 demethylases act in a global, stochastic manner.
the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting that H3K36 demethylases act in a global, stochastic manner.
the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting that H3K36 demethylases act in a global, stochastic manner.
the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner
The data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively
The data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively
The data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively
The data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively
The data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively
The data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively
The data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes despite disparate levels of H3K36 methylation.
Although genes showed disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes despite disparate levels of H3K36 methylation.
Although genes showed disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes despite disparate levels of H3K36 methylation.
Although genes showed disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes despite disparate levels of H3K36 methylation.
Although genes showed disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes despite disparate levels of H3K36 methylation.
Although genes showed disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes despite disparate levels of H3K36 methylation.
Although genes showed disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes despite disparate levels of H3K36 methylation.
Although genes showed disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
The data suggest that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency.
suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
The data suggest that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency.
suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
The data suggest that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency.
suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
The data suggest that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency.
suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
The data suggest that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency.
suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
The data suggest that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency.
suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
The data suggest that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency.
suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
The temporal data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively.
The temporal data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively.
The temporal data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively.
The temporal data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively.
The temporal data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively.
The temporal data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively.
The temporal data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively.
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay.
However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay.
However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay.
However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay.
However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay.
However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay.
However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay.
However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay
The study established rapid and reversible optogenetic control of the yeast Set2 methyltransferase by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The study established rapid and reversible optogenetic control of the yeast Set2 methyltransferase by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The study established rapid and reversible optogenetic control of the yeast Set2 methyltransferase by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The study established rapid and reversible optogenetic control of the yeast Set2 methyltransferase by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The study established rapid and reversible optogenetic control of the yeast Set2 methyltransferase by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The study established rapid and reversible optogenetic control of the yeast Set2 methyltransferase by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
The study established rapid and reversible optogenetic control of the yeast Set2 methyltransferase by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
Approval Evidence
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
Source:
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
Source:
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Source:
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Source:
The authors established rapid and reversible optogenetic control of yeast Set2 by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
Source:
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting directed deposition on all transcribed genes regardless of overall transcription frequency.
relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
Source:
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting that H3K36 demethylases act in a global, stochastic manner.
the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner
Source:
The data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively
Source:
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
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Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Source:
Relative rates of H3K36me3 accumulation were largely linear and consistent across genes despite disparate levels of H3K36 methylation.
Although genes showed disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes
Source:
Light activation caused efficient nuclear localization of Set2-LANS followed by H3K36me3 deposition in vivo.
Light activation resulted in efficient Set2-LANS nuclear localization followed by H3K36me3 deposition in vivo
Source:
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Source:
The data suggest that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency.
suggesting that H3K36me3 deposition occurs in a directed fashion on all transcribed genes regardless of their overall transcription frequency
Source:
The temporal data support transcription-dependent H3K36 methylation deposition and transcription-independent H3K36 methylation removal mechanisms.
Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggests transcription-dependent and -independent mechanisms for H3K36me deposition and removal, respectively.
Source:
The per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay.
However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay
Source:
The study established rapid and reversible optogenetic control of the yeast Set2 methyltransferase by fusing Set2 to the LANS domain.
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
Source:
Comparisons
Source-backed strengths
The reported engineering result is rapid and reversible optogenetic control of Set2 achieved by fusion to LANS. The system was applied in vivo in yeast, and the associated study linked H3K36me3 levels with RNA abundance and identified strong dependence of H3K36me3 removal on the demethylase Rph1.
Source:
We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain.
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