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Analysis of Allelic bias in gDNA, cDNA and ChIP with H3K27me3 and H3K36me3 antibody with multiplexed padlock probe approach

ABSTRACT: In this experiment, we asked how the allelic distribution of the active and repressive chromatin marks in clonal cell lines relates to the transcriptional allelic bias. A multiplexed padlock probe approach (Zhang et al., 2009) enabled us to assess allelic bias in heterozygous exonic SNPs in two clones with GM12878 genotype, and four clones from GM13130 cells. We used this approach to assess allelic bias in H3K27me3 and H3K36me3 ChIP samples simultaneously with cDNA from the same cells, as well as ChIP input and genomic DNA controls. In order to pool data from two individuals, one of which (GM13130) lacked complete genotypes for parents, we assessed SNP bias as reference and alternative alleles (rather than maternal or paternal bias). SNPs in cDNA were assigned to one of three bins: reference allele bias; no bias; and alternative allele bias. For these groups, allelic bias in H3K27me3 (Fig.4B) and H3K36me3 (Fig.4C) was determined. In unbiased loci, both H3K27me3 and H3K36me3 were equally represented. In contrast, preferential expression of an allele was associated with elevated levels of H3K36me3 and decreased levels of H3K27me3 on that allele. Both effects were highly significant (p<2x10e-9). Genes predicted to have MAE were about four-fold over-represented among genes where SNPs showed significant bias (Fig.4D). SNPs with skewed H3K27me3 and H3K36me3 distribution were highly enriched in the genes predicted as MAE (p<10e-6 and p=0.01, respectively; two-tailed Fisher's exact test). This suggests that the asymmetric distribution of the histone modifications is to a large extent due to the genes that have the chromatin signature of monoallelic expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53628 | GEO | 2014/02/07

REPOSITORIES: GEO

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Analysis of Allelic bias in gDNA, cDNA and ChIP with H3K27me3 and H3K36me3 antibody with multiplexed padlock probe approach

Project description:In this experiment, we asked how the allelic distribution of the active and repressive chromatin marks in clonal cell lines relates to the transcriptional allelic bias. A multiplexed padlock probe approach (Zhang et al., 2009) enabled us to assess allelic bias in heterozygous exonic SNPs in two clones with GM12878 genotype, and four clones from GM13130 cells. We used this approach to assess allelic bias in H3K27me3 and H3K36me3 ChIP samples simultaneously with cDNA from the same cells, as well as ChIP input and genomic DNA controls. In order to pool data from two individuals, one of which (GM13130) lacked complete genotypes for parents, we assessed SNP bias as reference and alternative alleles (rather than maternal or paternal bias). SNPs in cDNA were assigned to one of three bins: reference allele bias; no bias; and alternative allele bias. For these groups, allelic bias in H3K27me3 (Fig.4B) and H3K36me3 (Fig.4C) was determined. In unbiased loci, both H3K27me3 and H3K36me3 were equally represented. In contrast, preferential expression of an allele was associated with elevated levels of H3K36me3 and decreased levels of H3K27me3 on that allele. Both effects were highly significant (p<2x10e-9). Genes predicted to have MAE were about four-fold over-represented among genes where SNPs showed significant bias (Fig.4D). SNPs with skewed H3K27me3 and H3K36me3 distribution were highly enriched in the genes predicted as MAE (p<10e-6 and p=0.01, respectively; two-tailed Fisher's exact test). This suggests that the asymmetric distribution of the histone modifications is to a large extent due to the genes that have the chromatin signature of monoallelic expression. Samples analyzed were A. polyclonal cell line GM12878 , and clones derived from it: DF1 and DF2, B. Polyclonal GM13130 (H0) and clones derived from it: H7, H14 and H16. gDNA, cDNA, ChIP material and input were used.

2014-02-07 | E-GEOD-53628 | biostudies-arrayexpress

Whole RNA-seq on clones of GM12878 lymphoblastoid clones DF1 and DF2

Project description:Analysis of Allelic bias in clonal lymphoblastoid cells. Abstract: In mammals, numerous autosomal genes are subject to mitotically stable monoallelic expression (MAE), including genes that play critical roles in a variety of human diseases. Due to challenges posed by the clonal nature of MAE, very little is known about its regulation; in particular, no molecular features have been specifically linked to MAE. Here we report an approach that distinguishes MAE genes in human cells with great accuracy: a chromatin signature consisting of chromatin marks associated with active transcription (H3K36me3) and silencing (H3K27me3) simultaneously occurring in the gene body. The MAE signature is present in ~20% of ubiquitously expressed genes and over 30% of tissue-specific genes across cell types. Notably, it is enriched among key developmental genes that have bivalent chromatin structure in pluripotent cells. Our results open a new approach to the study of MAE that is independent of polymorphisms, and suggest that MAE is linked to cell differentiation.

2013-12-31 | GSE52090 | GEO

Whole RNA-seq on clones of GM12878 lymphoblastoid clones DF1 and DF2

2013-12-31 | E-GEOD-52090 | biostudies-arrayexpress

Mechanism of monoallelic expression and allelic rheostat role of DNA methylation (RRBS)

Project description:In mammalian cells, large groups of genes show epigenetically controlled unequal transcription of maternal and paternal alleles. Thousands of autosomal genes subject to monoallelic expression (MAE) comprise the largest such group. The initial random allelic choice in these loci is followed by mitotically stable transmission of the allele-specific state, leading to stable epigenetic and functional differences between clonal cell lineages. Molecular mechanisms underpinning MAE maintenance are not known. We devised and performed a drug screen for reactivation of epigenetically silenced alleles in mouse cells, using a new strategy based on deep targeted allele-specific RNA sequencing, which can read out multiple loci simultaneously. We found that, contrary to previous observations, DNA methylation plays a key role in mitotic memory of MAE in multiple autosomal loci. Having established that a specific perturbation can affect multiple loci, we assessed genome-wide impact of the drug exposure in several clonal cell lines, identifying over 600 genes with allele-specific expression changing with DNA methylation. We found that multiple distinct states of allele-specific expression correspond to the extent of DNA methylation and can be stably maintained, indicating allelic rheostat role of DNA methylation. Our findings reveal a previously unappreciated interplay of genetic and epigenetic control of allele-specific expression and reinforce the role of such regulation in maintaining differences between developmentally equivalent clonal cell lineages.

2023-09-20 | GSE144006 | GEO

Identification of mechanism of monoallelic expression and allelic rheostat role of DNA methylation

2022-10-06 | GSE144007 | GEO

Genome-wide characterization of allelic chromatin in human fibroblast and lymphoblastoid cell lines by high-density allele-specific analyses

Project description:Cis-regulatory variants are predicted to mediate the majority of the common genetic risk associated to complex disease, yet the specific causal variants have thus far been poorly characterized. Allele-specific (AS) assessment of chromatin modifications has the potential to elucidate specific cis-regulatory mechanisms. However, development of chromatin landscapes at allelic resolution has been challenging since sites of variable signal strength require substantial read depth not commonly applied in next-generation sequencing based approaches. In this study, we addressed this by directly assessing AS chromatin states through parallel analyses of input DNA and chromatin immunoprecipitates (ChIP) on high-density Illumina genotyping arrays. Allele-specificity for the histone modifications H3K4me1, H3K4me3, H3K27ac, H3K27me3 and H3K36me3 was assessed using ChIP samples generated from 14 lymphoblast and 6 fibroblast cell lines. Allele-specificity of chromatin was assessed in 14 lymphoblast and 6 fibroblast cell lines by assaying PolII & histone ChIP samples (H3K4me1, H3K4me3, H3K27ac, H3K27me3, H3K36me3) in parallel with gDNA and cDNA on high-density Illumina genotyping arrays.

2013-10-18 | E-GEOD-51272 | biostudies-arrayexpress

Identification of transcriptome SNPs for assessing allele specific gene expression within a super-hybrid rice Xieyou9308

Project description:We identified 9325 reliable single nucleotide polymorphisms (SNPs) distributed throughout the genome, of which nearly 68% were represented in R9308 versus Xieqingzao B by CT and GA SNPs. This may indicate that DNA methylation, a heritable epigenetic mark, exists in the parents and their F1 hybrid. Of 2793 identified transcripts with consistent allelic biases, only 480 (17%) showed significant allelic biases during at least one stage, suggesting that trans effects may mediate most transcriptional differences in hybrid offspring. Approximately 67% and 62% of the 480 transcripts showed allelic expression biases towards the R9308 allele at tillering and heading stages, respectively. Transcripts with higher levels of gene expression in R9308 also exhibited R9308 allelic biases in the hybrid. In addition, 125 transcripts were identified with significant allelic expression biases at both stages, of which 74% showed allele expression biases towards the R9308 allele. R9308 alleles may tend to preserve their characteristic states of activity in the hybrid and may play an important role in hybrid vigor at both stages. The allelic expression of 355 transcripts was highly stage-specific, with divergent allelic expression patterns observed at different developmental stages. Many transcripts associated with stress resistance were differently regulated in the F1 hybrid. The results of this study would provide valuable information for further understanding molecular mechanisms of heterosis.

2014-05-16 | GSE43727 | GEO

Chromatin signature identifies monoallelic gene expression across mammalian cell types (ChIP-seq)

Project description:Monoallelic expression of autosomal genes (MAE) is a widespread epigenetic phenomenon which is poorly understood, due in part to current limitations of genome-wide approaches for assessing it. Recently, we reported that a specific histone modification signature is strongly associated with MAE, and demonstrated that it can serve as a proxy of MAE in human lymphoblastoid cells (Nag et al. Elife. 2013 Dec 31;2:e01256). Here, we use murine cells to establish that this chromatin signature is conserved between mouse and human, and is associated with MAE in every tested cell type. Our analyses reveal extensive conservation in the identity of MAE genes between the two species. By applying MAE chromatin signature analysis to a large number of cell and tissue types, we show that the MAE state remains consistent during terminal cell differentiation and is predominant among cell-type specific genes, suggesting a link between MAE and specification of cell identity. Chromatin immunoprecipitation with antibodies specific for histone modifications H3K27me3 and H3K36me3 and subsequent high-throughput sequencing were performed on fixed chromatin from a B-lymphoid clonal cell line, derived from 129S1/SvImJ x CAST/EiJ F1 mice and immortalized with Abelson murine leukemia virus.

2015-06-17 | E-GEOD-67380 | biostudies-arrayexpress

Identification of transcriptome SNPs for assessing allele specific gene expression within a super-hybrid rice Xieyou9308

2014-05-16 | E-GEOD-43727 | biostudies-arrayexpress

Disruption of RNAPII transcription elongation links Oncogenic splicing factor mutations to replciation stress and targetable alterations in chromatin landscape [H3K36me3 ChIP-Seq]

Project description:To investigate changes in the H3K36me3 distribution across different conditions, we peformed ChIP-seq using antibody against the H3K36me3 in K562 cells at 4 days after modified allele expression We then performed coverage plot analyses using data obtained from ChIP-seq from IP fractions to investigate H3K36me3 distribution changes

2024-03-12 | GSE254788 | GEO

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