Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355886 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5068900.fastq.gz | Fastqsanger.gz | |||
| SRR5068901.fastq.gz | Fastqsanger.gz | |||
| SRR5068902.fastq.gz | Fastqsanger.gz | |||
| SRR5068903.fastq.gz | Fastqsanger.gz | |||
| SRR5068894.fastq.gz | Fastqsanger.gz |
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Project description:Recognition of modified histones by “reader” proteins constitutes a key mechanism regulating diverse chromatin-associated processes important for normal and neoplastic development. For instance, bromodomain-containing proteins bind to acetylated histones and regulate chromatin dynamics and gene expression. We recently identified the YEATS domain as a novel acetyllysine-binding module; however, the functional importance of YEATS domain-containing proteins in human cancer remains largely unknown. Here we show that the YEATS2 gene is highly amplified in human non-small cell lung cancer (NSCLC) and is required for cancer cell growth and survival. Biochemical and crystal structural studies show that YEATS2 binds to acetylated histone H3, and the YEATS domain utilizes a serine-lined aromatic “sandwiching” cage for acetyllysine readout. ChIP-seq analyses in lung cancer cells reveal that the YEATS2-containing ATAC complex colocalizes with H3K27 acetylation (H3K27ac) on the promoters of actively transcribed genes. Depletion of YEATS2 or disruption of the interaction between its YEATS domain and acetylated histones reduces the ATAC complex-dependent promoter H3K9ac levels and deactivates the expression of essential genes, including the ribosomal protein-encoding genes, which are important for cancer cell growth and survival. Taken together, our study identifies YEATS2 as a histone H3K27ac specific reader that regulates a transcriptional program essential for NSCLC tumorigenesis.
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Project description:The intracellular O-linked N-acetylglucosamine (O-GlcNAc) modification is known to be enriched in the nucleus and in particular on chromatin, but many of its chromatin targets remain to be identified. Herein we demonstrate the O-GlcNAcylation of YEATS Domain Containing 2 (YEATS2), a subunit of the chromatin Ada-two-A-containing (ATAC) complex and a reader of histone H3K27ac. We show that YEATS2 interacts with the O-GlcNAc transferase (OGT) and further pinpoint its major O-GlcNAcylation site to be Thr604 using electron transfer dissociation mass spectrometry. O-GlcNAcylation promotes the chromatin association of YEATS2, and the affinity between YEATS2 and other ATAC components on chromatin, such as ZZZ3, GCN5 and PCAF. Downstream, YEATS2-T604A attenuated the ATAC-dependent histone H3K9ac levels and inactivated the expression of essential ribosomal genes as shown in chromatin immunoprecipitation assays. Further, xenograft experiments show that YEATS2 O-GlcNAcylation promotes lung cancer tumorigenesis. Our work reveals the critical role of YEATS2 O-GlcNAcylation in stabilizing the ATAC complex on chromatin and expands the chromatin substrates of OGT.
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Project description:Phosphates and tensin homolog (PTEN) is a critical tumor suppressor, and even partial reduction of PTEN levels increases cancer susceptibility. PTEN loss frequently occurs in non-small cell lung carcinoma (NSCLC) and is associated with poor diagnosis. However, there are no effective interventions available to prevent or restore PTEN loss. CREB binding protein (CREBBP or CBP) is a well-known acetyltransferase. PTEN loss in lung cancer carrying CBP loss-of-function (LOF) mutations has not been addressed. Here, we showed that the decreased acetylation of histone deacetylase 3 (HDAC3) due to CBP LOF mutations contributes to PTEN loss in lung cancer. HDAC3 is a member of the class I histone deacetylase family. We found HDAC3 itself is acetylated by CBP at a previously unknown acetylation residue. Our data demonstrated that HDAC3 acetylation is required for gearing down HDAC3 activity and increasing the acetylation of histone proteins to promote the transcription of PTEN. Our findings suggest that HDAC3 acetylation is required for preserving the PTEN expression. The impaired HDAC3 acetylation in CBP LOF mutation lung cancer leads to PTEN loss and consequently promotes tumorigenesis and tumor resistance to chemotherapy. Our findings reveal epigenetic mechanisms of regulating PTEN expression and indicate HDAC3 is a potential target for restoring the tumor suppressor PTEN in CBP LOF mutation cancer.
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Project description:Recognition of histone acetylation by the GAS41 YEATS domain promotes H2A.Z deposition and tumorigenesis of non-small cell lung cancer
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Project description:Regulation of gene expression is an integral cellular process, fine-tuned by epigenetic marks like histone modifications. Perturbations in the activity or abundance of epigenetic factors can lead, or contribute to tumorigenesis in healthy cells. Remarkably, the addition of epigenetic marks is dependent on the metabolites produced during several essential cellular pathways. Here, we have explored the interplay between a highly expressed epigenetic factor YEATS2, and a metabolic enzyme GCDH in regulating epithelial to mesenchymal transition in head and neck cancer. We report the results of RNA-seq in YEATS2-silenced BICR10 cells to investigate the effect of YEATS2 in influencing gene expression globally. We have also performed ChIP-seq using YEATS2 antibody in BICR10 cells to obtain the globally occupied sites of YEATS2. Lastly, we report the changes in crotonylation at histone 3 lysine 27 (H3K27Cr) upon YEATS2 downregulation in BICR10 by performing ChIP-seq in shControl vs. shYEATS2 cells.
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Project description:AF9 Links Histone Acetylation to DOT1L-Mediated H3K79 Methylation
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