Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1232105 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR32599546_1.fastq.gz | Fastqsanger.gz | |||
| SRR32599546_2.fastq.gz | Fastqsanger.gz | |||
| SRR32599547_1.fastq.gz | Fastqsanger.gz | |||
| SRR32599547_2.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Define the chromatin remodelling induced by second generation HDACIs Outcome: We demonstrate that NKL54 treatment increased the number of H3K27ac peaks and caused a slight redistribution of H3K27ac peaks in promotorial regions. The hyperacetylation effect is evident in poorly acetylated loci, while hyperacetylated TSS turned out to be paradoxically deacetylated by NKL54 treatment. NKL54 caused a reduction in the binding of HDAC4 and HDAC9, especially at the intergenic regions. Instead, their binding to promoters was conserved. In contrast, NKL54 caused a dramatic increase in MEF2D binding to several genomic regions and especially to promoters. These new NKL54-enhanced MEF2D-chromatin interactions are often located at new genomic regions, whereas 40% of MEF2D peaks in untreated cells are conserved in NKL54-treated cells. Importantly, in these new regions, MEF2D is frequently recruited in the absence of HDAC4 or of HDAC9.
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