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ENL reads histone β-hydroxybutyrylation to modulate gene transcription (CUT&Tag)

ABSTRACT: ENL reads histone β-hydroxybutyrylation to modulate gene transcription (CUT&Tag)

PROVIDER: PRJNA1106475 | ENA |

REPOSITORIES: ENA

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ENL reads histone β-hydroxybutyrylation to modulate gene transcription (CUT&Tag)

Project description:Histone modifications are typically recognized by chromatin-binding protein modules (referred to as “readers”) to mediate fundamental processes such as transcription. Lysine β-hydroxybutyrylation (Kbhb) is a new type of histone mark that couples metabolism to gene expression. However, the readers that prefer histone Kbhb remain elusive. This knowledge gap must be filled in order to reveal the molecular mechanism of this epigenetic regulation. Herein, we developed a chemical proteomic approach, relying upon multivalent photoaffinity probes to capture binders of the mark and identified ENL as a novel target of H3K9bhb. Biochemical studies and CUT&Tag analysis further suggested that ENL favorably binds to H3K9bhb, and co-localizes with it on promoter regions to modulate gene expression. Notably, disrupting the interaction between H3K9bhb and ENL via structure-based mutation leads to the suppressed expression of the gene like MYC that drives cell proliferation.

2024-05-06 | GSE266268 | GEO

ENL reads histone β-hydroxybutyrylation to modulate gene transcription (RNA-Seq)

2024-05-06 | GSE266269 | GEO

ENL reads histone β-hydroxybutyrylation to modulate gene transcription (RNA-Seq)

Project description:ENL reads histone β-hydroxybutyrylation to modulate gene transcription (RNA-Seq)

| PRJNA1106487 | ENA

ENL reads histone β-hydroxybutyrylation to modulate gene transcription

Project description:Identification of hPTM binder through the chemoproteomic approach

2024-06-26 | PXD051689 | Pride

Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

Project description:Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

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Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

Project description:Gain-of-function mutations in the chromatin ‘reader’ ENL, identified in AML and Wilms tumor, have been shown to induce aberrant formation of transcriptional condensates in cellular systems. However, the precise role of these mutations and their condensate forming property in tumorigenesis remains unclear. By creating a conditional knock-in mouse model for the most prevalent ENL mutation, we establish ENL mutant as a bona fide oncogenic driver of acute myeloid leukemia in vivo. Heterozygous expression of ENL mutant perturbs the normal hematopoietic hierarchy and results in the aberrant expansion of myeloid progenitors with increased self-renewal property. Furthermore, the ENL mutant remodels histone modifications to alter differentiation processes and drive oncogenic gene expression during hematopoietic development. Importantly, targeted point mutagenesis to disrupt the condensate formation property completely abolishes ENL mutant’s oncogenic function in hematopoietic stem and progenitor cells (HSPCs). Lastly, short-term treatment with a small molecule inhibitor that blocks the acetyl-binding activity of ENL mutant reverts its impact on chromatin and significantly delays leukemia development in mice. Our studies reveal the crucial biological function of mutation-induced transcriptional condensates in chromatin regulation and cancer in vivo and provide proof-of-concept for targeting of pathogenic condensates as a promising therapy for certain cancers.

2024-04-14 | GSE239468 | GEO

HCT116_SMARCA4 CUT&Tag

Project description:HCT116_SMARCA4 CUT&Tag

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scNanoSeq-CUT&Tag: a long-read single-cell CUT&Tag sequencing method for efficient chromatin modification profiling within individual cells

Project description:We developed scNanoSeq-CUT&Tag, a streamlined method by adapting a modified CUT&Tag protocol to Oxford Nanopore sequencing platform for efficient chromatin modification profiling at single-cell resolution. We firstly tested the performance of scNanoSeq-CUT&Tag on six human cell lines: K562, 293T, GM12878, HG002, H9, HFF1 and adult mouse blood cells, it showed that scNanoSeq-CUT&Tag can accurately distinguish different cell types in vitro and in vivo. Moreover, scNanoSeq-CUT&Tag enables to effectively map the allele-specific epigenomic modifications in the human genome andallows to analyze co-occupancy of histone modifications. Taking advantage of long-read sequencing,scNanoSeq-CUT&Tag can sensitively detect epigenomic state of repetitive elements. In addition, by applying scNanoSeq-CUT&Tag to testicular cells of adult mouse B6D2F1, we demonstrated that scNanoSeq-CUT&Tag maps dynamic epigenetic state changes during mouse spermatogenesis. Finally, we exploited the epigenetic changes of human leukemia cell line K562 during DNA demethylation, it showed that NanoSeq-CUT&Tag can capture H3K27ac signals changes along DNA demethylation. Overall, we prove that scNanoSeq-CUT&Tag is a valuable tool for efficiently probing chromatin state changes within individual cells.

2024-09-06 | GSE249799 | GEO

CUT&Tag and BioCUT&Tag enables investigation of the AT-rich and dynamic epigenome of Plasmodium falciparum from low input samples

Project description:This study aimed to adapt CUT&Tag to Plasmodium falciparum samples as an efficient and sensitive alternative to classical ChIP-sequencing. We compare H3K9me3 and HP1 CUT&Tag with ChIP-seq datasets, showing successful establishment of CUT&Tag in P. falciparum. Next we aimed to scale down required input material for our CUT&Tag reactions and generated high-quality HP1 tracks with as little as 10.000 nuclei. To minimise potential sample loss we tested feasibility of utilising (frozen) saponin parasite isolates as input material instead of nuclei, which proved to be viable. Lastly, we deployed our new technique Dimerisation-induced Biotinylation-CUT&Tag (DiBioCUT&Tag) to catch transient interactions by biotinylation of strongly associated proteins such as histones. We tested this technique on HP1 and compared standart CUT&Tag with DiBioCUT&Tag. Furthermore, we explored interactions of the transcription factor BDP5, which we were previously unable to succesfully ChIP.

2024-06-27 | GSE270104 | GEO

MECP2 directly interacts with RNA polymerase II to modulate transcription in human neurons. [CUT&Tag]

Project description:MECP2 directly interacts with RNA polymerase II to modulate transcription in human neurons. [CUT&Tag]

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