NicE-seq in Suv39h2 knockdown 8-cell stage
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA576800 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10257064_1.fastq.gz | Fastqsanger.gz | |||
| SRR10257064_2.fastq.gz | Fastqsanger.gz | |||
| SRR10257065_1.fastq.gz | Fastqsanger.gz | |||
| SRR10257065_2.fastq.gz | Fastqsanger.gz | |||
| SRR10257066_1.fastq.gz | Fastqsanger.gz |
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Project description:Determination of accessible chromatin regions in the 8-cell stage mouse embryo after Suv39h2 knockdown The study aimed to address a potential function of H3K9me3 in early mouse development by assessing its impact on chromatin compaction. The histone methyltransferase responsible for de novo H3K9me3 at fertilization Suv39h2, was knocked down by microinjection of dsRNA targeting Suv39h2 in the early zygote. Embryos were then cultured until the 8-cell stage of development. They were then fixed and chromatin compaction was assessed by NicE-seq in pools of 10 8-cell stage embryos.
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Project description:Mammalian chromatin is dynamic and contains structural information that leads to transcriptional regulation of genes by recruiting transcription factors and altering nucleosome positioning. Here, we describe open chromatin mapping using Nicking Enzyme assisted sequencing (NicE-seq) for integrative epigenomic analysis. NicE-seq captures open chromatin sites in both fixed and native cells and reveals the genomic location of open chromatin sites (OCS) and transcription factor occupancy at single nucleotide resolution, with as few as 250 HCT116 cells. In HCT116 cells a large percentage of the OCS were coincident with DHS (DNaseI hypersensitive site) and ATAC-seq sites. OCSs correlated well with RNA pol II occupancy and transcriptionally active chromatin marks, while displaying a pattern contrasting to CpG methylation. ChIP CTCF peaks common to OCS and DHS displayed a strong correlation with H3K4me3 and H3K27ac marks. Further peaks unique to OCS and ChIP CTCF peaks also correlated strongly with H3K4me3, H3K27ac and higher transcription. Similar results were also obtained for Max and Sp1 transcription factors. Using NicE-seq we have demonstrated that HCT116 cells, treated with anti cancer drug decitabine, displayed time dependent accumulation of OCS coinciding with hypomethylation of the genome, particularly in SINE and satellite repetitive DNA. Differentially methylated regions (DMRs) were more pronounced in promoters, 5’UTR, CpG islands and exons. In summary, sequence specificity offered by a nicking enzyme allows a means to study open chromatin structure and hypomethylation of genomes, revealing the open chromatin landscape in cellular context.
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Project description:Breast cancer, the most prevalent malignancy among women, is predominantly estrogen receptor-positive (ER+), with ER+ cases accounting for 80% of the total. The combination of CDK4/6 inhibitors and endocrine therapy has become the standard treatment for advanced ER+ breast cancer. However, around 30% of patients exhibit intrinsic resistance, while others eventually develop acquired resistance leading to recurrence and metastasis. Here, we identified reduced exon 2 skipping of SUV39H2 in CDK4/6 inhibitor-resistant breast cancer cells, leading to increased SUV39H2 protein expression and consequent elevation of H3K9me3 levels, collectively suppressing the p53 pathway and promote resistance. Subsequently, we designed antisense oligonucleotides (ASOs) to modulate SUV39H2 exon skipping, which successfully reduced SUV39H2 levels and H3K9me3 modifications, thereby reactivating p53 target genes and restoring drug sensitivity in vitro and in vivo.Our results demonstrate that SUV39H2 serves as both a potential biomarker and therapeutic target for CDK4/6 inhibitor-resistant breast cancer, highlighting its clinical translational value.
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Project description:Breast cancer, the most prevalent malignancy among women, is predominantly estrogen receptor-positive (ER+), with ER+ cases accounting for 80% of the total. The combination of CDK4/6 inhibitors and endocrine therapy has become the standard treatment for advanced ER+ breast cancer. However, around 30% of patients exhibit intrinsic resistance, while others eventually develop acquired resistance leading to recurrence and metastasis. Here, we identified reduced exon 2 skipping of SUV39H2 in CDK4/6 inhibitor-resistant breast cancer cells, leading to increased SUV39H2 protein expression and consequent elevation of H3K9me3 levels, collectively suppressing the p53 pathway and promote resistance. Subsequently, we designed antisense oligonucleotides (ASOs) to modulate SUV39H2 exon skipping, which successfully reduced SUV39H2 levels and H3K9me3 modifications, thereby reactivating p53 target genes and restoring drug sensitivity in vitro and in vivo.Our results demonstrate that SUV39H2 serves as both a potential biomarker and therapeutic target for CDK4/6 inhibitor-resistant breast cancer, highlighting its clinical translational value.
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