Genome wide chromatin profile for Histone H1.4 (pan-H1.4) and Phosphorylated H1.4 (pS187-H1.4)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA566437 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10148985.fastq.gz | Fastqsanger.gz | |||
| SRR10148986.fastq.gz | Fastqsanger.gz | |||
| SRR10148987.fastq.gz | Fastqsanger.gz | |||
| SRR10148988.fastq.gz | Fastqsanger.gz | |||
| SRR10148989.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we use novel, highly specific custom antibodies against a linker histone variant and its modified form to conduct chromatin immunoprecipitation (ChIP) followed by Next Generation Sequencing (NGS) to investigate their binding profiles as a result of transcription inititation. Here we use an estrogen responsive breast cancer cell line, MCF7 to study the enrichment patterns of Histone H1.4 (pan-H1.4) and Phosphorylated H1.4 (pS187-H1.4) across the genome as a result of a short estrogen treatment (30 mins). We find that pS187-H1.4 is preferentially enriched at the promoters of active genes as opposed to the depletion of pan-H1.4 at the same site. Additionally, we use a short treatment of Flavopiridol- an inhibitory drug specific for Cyclin-dependent Kinase-9 (CDK9) which is responsible for the phosphorylation of H1.4 cells, to demonstrate the quenching of this signal at sites specificially activated as a result of the estrogen treatment. This demonstrates for the first time that pS187-H1.4 is associated with active genes and may even be involved in the regulation of gene activity.
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Project description:Rahman syndrome (RMNS) is a rare genetic disorder characterized by mild to severe intellectual disability, hypotonia, anxiety, autism spectrum disorder, vision problems, bone abnormalities, and dysmorphic facies. De novo heterozygous mutations in H1-4 encoding the linker histone H1.4 are found in individuals with RMNS; however, the underlying mechanisms causing significantly impaired neurodevelopment are not understood. So far, all neurodevelopmental associated mutations in H1-4 are small insertions or deletions that create a shared frameshift, resulting in a H1.4 protein that is both truncated and possessing an abnormal C-terminus frameshifted tail (H1.4 CFT). To expand understanding of mutations and phenotypes associated with mutant H1-4, we identified additional and new DNA variants at both the C- and N-terminus of H1.4. The clinical features of mutations identified at the C-terminus are consistent with other reports that strengthen the support of pathogenicity of H1.4 CFT. However, the pathogenicity of disrupting variants at the N-terminus could not be determined. To understand how H1.4 CFT may disrupt brain function, we exogenously expressed wildtype or H1.4 CFT protein in primary rat hippocampal neurons and assessed neuronal structure and function. Genome-wide transcriptome analysis revealed ~400 genes altered specifically in the presence of H1.4 CFT. Neuronal genes downregulated by H1.4 CFT were enriched for functional categories involved in synaptic communication and neuropeptide signaling. Neurons expressing H1.4 CFT showed reduced activity on extracellular electrode arrays, indicating that these transcriptional changes were sufficient to disrupt physiological neuronal function. These data are the first to characterize the consequence of H1.4 CFT in neurons. Our data provide initial insights into causes of neurodevelopmental impairments associated with these frameshift mutations in the C-terminus of H1.4 and highlight the need for future studies on the function of normal histone H1.4 in neurons.
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Project description:Linker histone H1 and the four nucleosomal histone proteins form the greater chromatosome superstructure of chromatin. While a critical component of the epigenetic landscape, the specific role of H1 has remained elusive due in part to compensation by other H1 family members, a lack of genome-wide analyses, and suitable model systems. Ablation of H1.4 in a human osteosarcoma line with high H1-4 expression resulted in broad changes in DNA accessibility as well as gene expression. Genes in critical signaling pathways are upregulated with H1.4 loss (RAR, acetylcholine/glutaminergic receptors) while extracellular matrix and collagen biosynthesis genes are repressed. The gene loci of the same critical pathways were enriched in differentially accessible chromatin after loss of H1.4, and many of this differential chromatin overlaps regions of known enhancer regions. The AP-1 binding motif was highly enriched at sites with reduced accessibility while sites with gained chromatin accessibility were enriched in more basal factor motifs (TBP, SRF). At sites of altered chromatin accessibility following H1.4-loss, concomitant changes to core histone proteins were observed (H3K27ac and H3K4me1), and the changes in PTMs was concordant with the change in accessibility. Alterations to chromatin accessibility and epigenetic activity were enriched at regions with known enhancer-like chromatin, and the size of the altered chromatin footprints were consistent with enhancer regions. Sites which gain chromatin accessibility localize to polycomb, heterochromatin and quiescent/low chromatin states, but were found to gain RNA transcription in cells lacking H1.4. Broad changes in chromatin accessibility and activity, as well as robust changes in gene transcription when H1.4 is abolished, place linker H1.4 as a hitherto underappreciated regulator of transcription response patterns as well as a dynamic member of regulatory chromatin.
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Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1.4 (sh120) or multiple H1 variants (sh225), or overexpressing WT or K26A mutant HA-tagged H1.4.
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Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1.4 (120sh) or multiple H1 variants (225sh)
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