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Internally Calibrated ChIP-seq (ICeChIP-seq) using a large panel of antibodies against H3K4 methylations to measure genome-wide histone modification density in mammalian cells

ABSTRACT: Internally Calibrated ChIP-seq (ICeChIP-seq) using a large panel of antibodies against H3K4 methylations to measure genome-wide histone modification density in mammalian cells

PROVIDER: PRJNA401866 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12684564_1.fastq.gz	Fastqsanger.gz
	SRR12684564_2.fastq.gz	Fastqsanger.gz
	SRR6010170_1.fastq.gz	Fastqsanger.gz
	SRR6010170_2.fastq.gz	Fastqsanger.gz
	SRR6010180_1.fastq.gz	Fastqsanger.gz

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Internally Calibrated ChIP-seq (ICeChIP-seq) using a large panel of antibodies against H3K4 methylations to measure genome-wide histone modification density in mammalian cells

Project description:Post-translational modifications (PTMs) on histone proteins regulate genome accessibility and are frequently studied using chromatin immunoprecipitation (ChIP). In ChIP, an antibody putatively specific towards a histone PTM is used to map its genomic locations. ChIP experiments assume perfect antibody-epitope specificity, an assumption previously shown to be problematic, largely through peptide array studies. Among the most well-studied histone PTMs are the mono-, di-, and tri-methylation states of histone H3 lysine 4 (H3K4). While each state has been ascribed different biological functions, the methylation state specificity of antibodies used in these studies has not been systematically interrogated. Here, we use internally calibrated ChIP (ICeChIP) to comprehensively define the specificities of 52 commercially available antibodies marketed to distinguish the three methylation states of H3K4, allowing identification of both high- and low-specificity antibodies. We then conduct ICeChIP-seq with 18 such antibodies of varying specificity. We further find that the sum of H3K4me1 and H3K4me2 across enhancers contacting a promoter correlates strongly with gene expression for all genes, including housekeeping genes, and note that use of low-quality antibodies yields materially different biological interpretations. These results illustrate the way by which variable specificity of commercial antibodies contributes to the “reproducibility crisis” in biological research and demonstrates the need to carefully validate antibodies with techniques appropriate for the intended applications.

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Project description:Histone methylations play a major role in regulating the chromatin state and gene expression, yet little is known about their involvement in differential gene expression and function of memory CD8 T cells. Here, we report a genome-wide analysis of two histone H3 methylations (H3K4me3 and H3K27me3) and gene expression in naïve, central (TCM) and effector (TEM) memory CD8 T cells. Analysis of 16,314 annotated genes in CD8 T cell subsets revealed that gene expression were positively correlated with the levels of H3K4me3 and negatively correlated with the levels of H3K27me3 in these gene loci. The correlation between differential H3K4me3 orH3K27me3 levels with gene expressions in memory CD8 T cells displayed four distinct modes: repressive, active, poised, and bivalent, reflecting their complex regulation and different function of these genes. Furthermore, accessible chromatin states of different gene loci were preferentially influenced by different histone modifications as demonstrated here high levels of H3K9ac found in active gene loci without high levels of H3K4me3. These findings reveal a histone methylation based complex regulation of differential gene expression in memory CD8 T cells. Thus, change of chromatin structure mediated by histone methylation may serve a fundamental basis for the rapid transcriptional response of memory CD8 T cells. genome-wide analysis of two histone H3 methylations (H3K4me3 and H3K27me3) in naïve, central (TCM) and effector (TEM) memory CD8 T cells.

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Calibrated ChIP-seq for Xist-mediated polycomb recruitment

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Project description:The spatiotemporal regulation of gene expression is central for cell-lineage specification during embryonic development and is achieved through the combinatorial action of transcription factors/co-factors and epigenetic states at cis-regulatory elements. Here, we show that in addition to implementing H3K4me3 at promoters of bivalent genes, Mll2 (KMT2B)/COMPASS can also implement H3K4me3 at a subset of non-TSS regulatory elements, a subset of which shares epigenetic signatures of active enhancers. Our mechanistic studies reveal that association of Mll2's CXXC domain with CpG-rich regions plays an instrumental role for chromatin targeting and subsequent implementation of H3K4me3. Although Mll2/COMPASS is required for H3K4me3 implementation on thousands of loci, generation of catalytically mutant MLL2/COMPASS demonstrated that H3K4me3 implemented by this enzyme was essential for expression of a subset of genes, including those functioning in the control of transcriptional programs during embryonic development. Our findings suggest that not all H3K4 trimethylations implemented by MLL2/COMPASS are functionally equivalent.

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