Epigenetics
Histone acylations respond to plant stress
Open access · cc by · source: Europe PMC
Rice histone butyrylation and crotonylation mark active chromatin and shift under starvation/submergence.
Study at a glance
- Design
- Animal / in-vitro — MS and ChIP-seq mapping of histone Kbu/Kcr in rice vs H3K9ac under metabolic stress
- N
- Plant chromatin proteomics/ChIP-seq study — no single primary analytic N in stored text
- Population
- Rice (and related plants) under stress conditions
- Outcome
- Distribution and stress dynamics of histone butyrylation/crotonylation
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
Many Kcr sites on H3/H4; Kbu/Kcr resemble acetylation distribution and change with metabolic stress.
Methodology
Mapped Kbu/Kcr sites by MS and ChIP-seq in rice and compared to H3K9ac with transcriptomes under stress.
Limitations
Does not prove every site is required for a specific stress phenotype.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Several papers tagged for this method barely use qPCR as the headline assay. Cryptosporidium oocyst work is a transcriptome of environmental persistence; FECR1 function was tested with dCas9 chromatin immunoprecipitation and TET1/DNMT1 regulation in MDA-MB231 cells; rice histone Kbu/Kcr maps came from mass spectrometry and ChIP-seq. Any qPCR in those studies is at most a supporting check.
Evidence for the claim as stated.
Lexicon tagging also pulls in studies whose core methods are RNA-seq, CasIP or ChIP-seq/MS. Cryptosporidium metabolic inferences, FECR1 promoter RNA pull-downs, and rice histone acylations should not be read as qPCR papers that measured the same class of target.
Evidence for the claim as stated.
Many papers in the CRISPR index mention CRISPR or Cas proteins in passing while the actual experiment is something else (APEX2 proximity labelling, pan-genome presence/absence, ChIP-seq of histone acylations, scRNA-seq of endoderm). Those hits show why a body-count lexicon over-recruits; they are not additional editing results.
Evidence for the claim as stated.
In rice, MS plus ChIP-seq mapped histone lysine butyrylation and crotonylation: many Kcr sites on H3/H4, with Kbu/Kcr resembling acetylation distribution and changing with metabolic stress. Occupancy dynamics are not proof that every site is required for a named stress phenotype.
Evidence for the claim as stated.
Genuine MS designs still disagree about what is being counted. APEX2 inventories membrane-face neighbours in living cells (22 OMM; 72 ERM); caveolar work quantifies a purified coat; Rab5 work maps three ubiquitin lysines; rice work maps histone acylations under stress. A 'proteomics paper' can be spatial, stoichiometric, or epigenetic, and those outputs are not interchangeable.
Evidence for the claim as stated.
Rice histone lysine butyrylation and crotonylation were mapped by mass spectrometry and ChIP-seq and compared with H3K9ac and stress transcriptomes. Many Kcr sites sit on H3/H4; Kbu/Kcr resemble acetylation distribution and change with metabolic stress. The maps do not prove every site is required for a specific stress phenotype.
Evidence for the claim as stated.
Only the rice histone-acylation paper is clearly genome-wide ChIP-seq of chromatin marks (Kbu/Kcr versus H3K9ac under stress). Foxp3 work is candidate-locus ChIP; FECR1 is CasIP of promoter RNAs; Yoruba data are 27K methylation arrays. Treating them as one ChIP-seq method overstates shared technology.
Evidence for the claim as stated.
What 'epigenetic activation' means also disagrees. Rice Kcr occupancy resembles acetylation and moves with metabolic stress but is not proven necessary at each site. FECR1 recruits TET1/DNMT1 logic at FLI1. Foxp3 stability tracks TSDR demethylation rather than a mapped histone peak. Those are different causal sketches.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Lexicon tagging also pulls in studies whose core methods are RNA-seq, CasIP or ChIP-seq/MS. Cryptosporidium metabolic inferences, FECR1 promoter RNA pull-downs, and rice histone acylations should not be read as qPCR papers that measured the same class of target.
Genuine MS designs still disagree about what is being counted. APEX2 inventories membrane-face neighbours in living cells (22 OMM; 72 ERM); caveolar work quantifies a purified coat; Rab5 work maps three ubiquitin lysines; rice work maps histone acylations under stress. A 'proteomics paper' can be spatial, stoichiometric, or epigenetic, and those outputs are not interchangeable.
- Supports · Mapping the faces of mitochondria and ER
- Supports · What proteins build the caveolar coat?
- Supports · How does monoubiquitin turn down Rab5?
Only the rice histone-acylation paper is clearly genome-wide ChIP-seq of chromatin marks (Kbu/Kcr versus H3K9ac under stress). Foxp3 work is candidate-locus ChIP; FECR1 is CasIP of promoter RNAs; Yoruba data are 27K methylation arrays. Treating them as one ChIP-seq method overstates shared technology.
- Supports · Epigenetic locking of Foxp3 in Tregs
- Supports · FLI1 circRNA FECR1 drives metastasis
- Supports · Genetics shapes methylation and expression
What 'epigenetic activation' means also disagrees. Rice Kcr occupancy resembles acetylation and moves with metabolic stress but is not proven necessary at each site. FECR1 recruits TET1/DNMT1 logic at FLI1. Foxp3 stability tracks TSDR demethylation rather than a mapped histone peak. Those are different causal sketches.
- Supports · FLI1 circRNA FECR1 drives metastasis
- Supports · Epigenetic locking of Foxp3 in Tregs
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Same topic cluster — not a recommendation engine.