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Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [ChIP-seq]

ABSTRACT: The intestinal epithelium undergoes rapid turnover driven by Lgr5+ intestinal stem cells (ISCs) at the crypt base, and can recover despite ISC loss during damage. However, the role of epigenetic modifications in regulating this regeneration remains unclear. In this study, we report that H3K14 crotonylation (H3K14cr), a vital histone modification mediated by the acyltransferase HBO1, is essential for intestinal regeneration. HBO1 ablation in the intestinal epithelium exacerbates dextran sulfate sodium (DSS)-induced colitis.

ORGANISM(S): Mus musculus

PROVIDER: GSE278970 | GEO | 2025/08/13

REPOSITORIES: GEO

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Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [RNA-seq]

Project description:The intestinal epithelium undergoes rapid turnover driven by Lgr5+ intestinal stem cells (ISCs) at the crypt base, and can recover despite ISC loss during damage. However, the role of epigenetic modifications in regulating this regeneration remains unclear. In this study, we report that H3K14 crotonylation (H3K14cr), a vital histone modification mediated by the acyltransferase HBO1, is essential for intestinal regeneration. HBO1 ablation in the intestinal epithelium exacerbates dextran sulfate sodium (DSS)-induced colitis.

2025-08-13 | GSE279059 | GEO

Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury

Project description:This SuperSeries is composed of the SubSeries listed below.

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The Epigenetic Regulator PHF16 Redresses Homeostasis During Intestinal Injury Repair [RNA-seq]

Project description:The intestinal stem cells (ISCs) are highly vulnerable to DNA damage, being in a constant state of proliferation1. Reserve crypt stem cells restore homeostatic intestinal epithelium following damage-induced ablation of ISCs2-5. Here, we report that the epigenetic regulator PHD finger protein 16 (PHF16) redresses revival stem cell (revSC) activity after damage repair. Phf16-/Y mice showed defects in exit from the regenerative state of revSCs and failed in intestinal crypt regeneration, while they still induced revSCs in response to tissue damage, as observed using single-cell RNA-sequencing. RNA-sequencing and ATAC-sequencing analyses of Phf16-/Y intestinal organoids revealed that PHF16 controls intestinal epithelial differentiation by promoting HBO1-mediated histone H3K14 acetylation, while PHF16 also counteracts YAP/TAZ activity by ubiquitination of CDC73, faithfully reverting damage-induced revSCs to homeostatic gut epithelial cells. Together, our findings demonstrate the importance of timely suppression of regenerative activity by PHF16 for the restoration of gut homeostasis after acute tissue injury.

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The Epigenetic Regulator PHF16 Redresses Homeostasis During Intestinal Injury Repair

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Histone crotonylation

Project description:Histone crotonylation

| PRJNA535529 | ENA

SETDB1 activity is globally directed by H3K14 acetylation via its Triple Tudor Domain

Project description:SETDB1 is a major H3K9 methyltransferase. It contains a unique Triple Tudor Domain (3TD) which specifically bind the dual modification of H3K14ac in the presence of H3K9me1/2/3. In this study, we explored the role of the 3TD H3K14ac interaction in the H3K9 methylation activity by SETDB1. We generated the 3TD binding reduced F332A mutant and demonstrate in biochemical methylation assays on recombinant nucleosomes containing H3K14ac analogs, that H3K14 acetylation is crucial for the 3TD mediated recruitment of SETDB1. We also see this effect in the cells where SETDB1 binding and activity was globally correlated with H3K14ac, and knock-out (KO) of the H3K14 acetyltransferase HBO1 caused a drastic reduction in the H3K9me3 levels at SETDB1 dependent sites. Further analyses revealed that 3TD was not required for SETDB1 recruitment for regions targeted by KAP1, but at specific target regions, SETDB1 KO could not be efficiently reconstituted by a 3TD mutant of SETDB1 as shown by the finding that H3K9 methylation of L1M repeat elements is highly dependent on an intact 3TD. In summary, our data demonstrate an important role of the 3TD interaction with H3 tails containing K14ac and K9 methylation in the recruitment of SETDB1 to chromatin which is particularly relevant at L1M repeats.

2024-11-15 | GSE261744 | GEO

P300 Regulates Histone Crotonylation and Preimplantation Embryo Development (RNA-Seq)

Project description:Histone lysine crotonylation is a non-acetyl histone lysine modification that is evolutionarily conserved. It plays an important role in regulating various biological processes, including gene transcriptional regulation, spermatogenesis, and cell cycle. However, the dynamic changes and functions of histone crotonylation in preimplantation embryonic development in mammals remain unclear. In this study, we have shown that the transcription coactivator P300 functions as a writer of histone crotonylation during embryonic development. Depletion of P300 resulted in significant developmental defects and dysregulation of the transcriptome of embryos. Importantly, we demonstrated that P300 catalyzes the crotonylation of histone, directly stimulating transcription and regulating gene expression, thereby ensuring successful embryo development to the blastocyst stage. Furthermore, it is showed that the histone H3 lysine 18 crotonylation (H3K18cr) modification is predominantly located in active promoter regions. It serves as an epigenetic hallmark of key transcriptional regulators and promotes the transcription activation of genes. Together, our results propose a model wherein P300-mediated histone crotonylation plays a crucial role in regulating the fate of embryonic development.

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P300 Regulates Histone Crotonylation and Preimplantation Embryo Development (ChIP-Seq)

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Investigating the requirement of H3K14 and H3P16 for optimal H3K4me3

Project description:ChIP-seq experiment for histone H3 and H3K4me3 from wild-type Saccharomyces cerevisiae (WT) and strains in which H3K14 has been substituted for alanine (K14A) or H3P16 has been substituted with valine (P16V).

2014-07-22 | E-MTAB-2717 | biostudies-arrayexpress

Crotonylation of GAPDH regulates human embryonic stem cell endodermal lineage differentiation and metabolic switch

Project description:Post-translational modifications of proteins are crucial to the regulation of their activity and function. As a newly discovered acylation modification, crotonylation of non-histone proteins remains largely unexplored, particularly in human embryonic stem cells (hESCs). Here we report the investigation of induced crotonylation in hESCs, which resulted in hESCs of different pluripotency states differentiating into the endodermal lineage. We showed that increased protein crotonylation in hESCs was accompanied by transcriptomic shifts and decreased glycolysis. Through large-scale profiling of non-histone protein crotonylation, we showed that metabolic enzymes were major targets of inducible crotonylation in hESCs. We further discovered GAPDH as a key glycolytic enzyme regulated by crotonylation during endodermal differentiation from hESCs, where crotonylation of GAPDH decreased its enzymatic activity thereby leading to reduced glycolysis. Our study demonstrates that crotonylation of glycolytic enzymes may be crucial to metabolic switching and cell fate determination in hESCs.

2022-10-03 | GSE214619 | GEO

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