Source 1primary paper2020
Toolkit/light activated nuclear shuttle (LANS) domain
light activated nuclear shuttle (LANS) domain
Also known as: LANS, LANS domain
Taxonomy: Mechanism Branch / Component. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
The light-activated nuclear shuttle (LANS) domain is a protein domain used as a fusion module to confer light-controlled subcellular localization. In the cited 2020 yeast study, fusion of LANS to the Set2 methyltransferase enabled rapid and reversible optogenetic control of Set2 function.
Usefulness & Problems
Why this is useful
LANS is useful for imposing optical control over the localization and activity of a fused protein, allowing temporal perturbation of nuclear processes. In the cited application, it enabled dynamic control of Set2 to study transcription-dependent and transcription-independent H3K36 methylation dynamics in yeast.
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.
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
This tool addresses the need for rapid and reversible control of Set2 activity without permanent genetic disruption. The reported use case specifically enabled dissection of H3K36me2/3 deposition and removal dynamics, including dependence of H3K36me3 loss on the demethylase Rph1.
Problem links
Need precise spatiotemporal control with light input
DerivedThe light-activated nuclear shuttle (LANS) domain is a protein domain used to confer optogenetic control over protein localization by fusion to a target protein. In the cited work, fusion of LANS to the yeast Set2 methyltransferase enabled rapid and reversible light-controlled regulation of Set2 activity.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Component: A low-level protein part used inside a larger architecture that realizes a mechanism.
Mechanisms
light-dependent nuclear shuttlinglight-dependent nuclear shuttlingreversible optogenetic controlreversible optogenetic control via protein-domain fusionTechniques
No technique tags yet.
Target processes
No target processes tagged yet.
Input: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementoperating role: actuatorswitch architecture: single chain
The demonstrated implementation was achieved by fusing the target enzyme Set2 to the LANS domain in yeast. The supplied evidence does not provide construct architecture, linker design, expression system details beyond the yeast context, or any required cofactors.
The supplied evidence documents LANS only in a single reported application involving yeast Set2. The evidence provided does not specify illumination wavelength, kinetic constants, structural design details, or validation across additional cargos, organisms, or cellular compartments.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2primary paper2020Genome Research
Source 3primary paper2024UNC Libraries
Ranked Claims
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.
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Total H3K36me3 levels correlated with RNA abundance.
with total H3K36me3 levels correlating with RNA abundance
Section: abstract
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and highly dependent on the demethylase Rph1.
Removal of H3K36me2/3 was rapid and highly dependent on the demethylase Rph1.
Removal H3K36me2/3 was also rapid and 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.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Removal of H3K36me3 was highly dependent on the demethylase Rph1.
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
Early H3K36me3 dynamics showed rapid methylation in vivo, and total H3K36me3 levels correlated with RNA abundance.
Early H3K36me3 dynamics identified rapid methylation in vivo , with total H3K36me3 levels correlating with RNA abundance.
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Across genes, relative rates of H3K36me3 accumulation were largely linear and consistent, suggesting a rate-limiting mechanism for H3K36me3 deposition.
Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting a rate-limiting mechanism for H3K36me3 deposition.
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.
However, 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.
However, 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.
However, 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.
However, 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.
However, 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.
However, 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.
However, 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.
However, 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.
However, 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.
However, 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 suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
The data suggest that H3K36 demethylases act in a global, stochastic manner.
suggesting H3K36 demethylases act in a global, stochastic manner
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
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
Section: abstract
The authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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 authors 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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
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.
Section: abstract
Approval Evidence
3 sources3 linked approval claimsfirst-pass slug light-activated-nuclear-shuttle-lans-domain
by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain
Source:
by fusing the enzyme with the light activated nuclear shuttle (LANS) domain
Source:
by fusing the enzyme with the light-activated nuclear shuttle (LANS) domain
Source:
engineering resultsupports
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:
tool establishmentsupports
The authors 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:
tool establishmentsupports
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 cited work reports that LANS fusion established rapid and reversible optogenetic control of yeast Set2. This temporal control supported mechanistic observations linking total H3K36me3 levels with RNA abundance and showing that removal of H3K36me2/3 and H3K36me3 was highly dependent on 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.
Compared with CRY2 C-terminal tail
light activated nuclear shuttle (LANS) domain and CRY2 C-terminal tail address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Strengths here: appears more independently replicated; looks easier to implement in practice.
Compared with H3K27me3
light activated nuclear shuttle (LANS) domain and H3K27me3 address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Strengths here: appears more independently replicated; looks easier to implement in practice.
light activated nuclear shuttle (LANS) domain and photoactivatable inhibitor for myosin light chain kinase (MLCK) address a similar problem space.
Shared frame: same top-level item type; same primary input modality: light
Strengths here: appears more independently replicated; looks easier to implement in practice.
Ranked Citations
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