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Epigenomics ag chip seq data
Overview of Deep5hmC. ( A ) The training set of Deep5hmC can be derived from matched 5hmC-seq and other epigenetic data such as <t>histone</t> <t>ChIP-seq</t> or DNase-seq/ATAC-seq from one condition. Specifically, the 5hmC-seq data can be collected from tissue-specific human tissues, which include bladder, brain, breast, heart, kidney, liver, lung, marrow, ovary (female), pancreas, placenta (female), prostate (male), colon (sigmoid), colon (transverse), skin, stomach, and testis (male). The matched tissue-specific epigenetic data, such as histone ChIP-seq data profiling histone modification and DNase-seq/ATAC-seq profiling chromatin accessibility, can be collected from public consortiums such as Roadmap Epigenomics and ENCODE. In this context, Deep5hmC aims to predict genome-wide 5hmC modification in a single condition. ( B ) The training set of Deep5hmC can also be derived from matched 5hmC-seq and ChIP-seq from a case–control study (e.g. Alzheimer’s disease (AD) versus healthy control) for predicting differentially hydroxymethylated regions (DhMRs). ( C ) Deep5hmC is a multimodal deep learning model to improve the prediction of tissue/cell type-specific genome-wide 5hmC modification by leveraging both DNA sequence and epigenetic features such as histone modification and chromatin accessibility. Deep5hmC consists of four modules, including Deep5hmC-binary, Deep5hmC-cont, Deep5hmC-gene, and Deep5hmC-diff. Specifically, Deep5hmC-binary takes the labeled 5hmC peaks and non-peaks as the training set to identify the 5hmC-enriched regions. Deep5hmC-cont takes the normalized read counts in 5hmC peaks and aims to predict the continuous 5hmC modification genome-wide. By leveraging Deep5hmC-cont, Deep5hmC-gene aggregates the predictions of Deep5hmC-cont in the gene bodies as the surrogate for the predicted gene expression. Different from Deep5hmC-binary, Deep5hmC-diff takes the labeled DhMRs/non-DhMRs in a case–control design of 5hmC-seq as the training set to predict genome-wide DhMRs and may discover de novo DhMRs. ( D ) Model architecture of Deep5hmC. Deep5hmC consists of both sequence modality and epigenetic modality consisting of their own convolutional neural networks (CNNs) to derive separate feature representations, which will be joined later via the multi-modal factorized bilinear (MFB) pooling fusion layer. The output of the MFB fusion layer will further connect to fully connected layers and the output layer afterward.
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Article Title: Deep5hmC: predicting genome-wide 5-hydroxymethylcytosine landscape via a multimodal deep learning model

Journal: Bioinformatics

doi: 10.1093/bioinformatics/btae528

Overview of Deep5hmC. ( A ) The training set of Deep5hmC can be derived from matched 5hmC-seq and other epigenetic data such as histone ChIP-seq or DNase-seq/ATAC-seq from one condition. Specifically, the 5hmC-seq data can be collected from tissue-specific human tissues, which include bladder, brain, breast, heart, kidney, liver, lung, marrow, ovary (female), pancreas, placenta (female), prostate (male), colon (sigmoid), colon (transverse), skin, stomach, and testis (male). The matched tissue-specific epigenetic data, such as histone ChIP-seq data profiling histone modification and DNase-seq/ATAC-seq profiling chromatin accessibility, can be collected from public consortiums such as Roadmap Epigenomics and ENCODE. In this context, Deep5hmC aims to predict genome-wide 5hmC modification in a single condition. ( B ) The training set of Deep5hmC can also be derived from matched 5hmC-seq and ChIP-seq from a case–control study (e.g. Alzheimer’s disease (AD) versus healthy control) for predicting differentially hydroxymethylated regions (DhMRs). ( C ) Deep5hmC is a multimodal deep learning model to improve the prediction of tissue/cell type-specific genome-wide 5hmC modification by leveraging both DNA sequence and epigenetic features such as histone modification and chromatin accessibility. Deep5hmC consists of four modules, including Deep5hmC-binary, Deep5hmC-cont, Deep5hmC-gene, and Deep5hmC-diff. Specifically, Deep5hmC-binary takes the labeled 5hmC peaks and non-peaks as the training set to identify the 5hmC-enriched regions. Deep5hmC-cont takes the normalized read counts in 5hmC peaks and aims to predict the continuous 5hmC modification genome-wide. By leveraging Deep5hmC-cont, Deep5hmC-gene aggregates the predictions of Deep5hmC-cont in the gene bodies as the surrogate for the predicted gene expression. Different from Deep5hmC-binary, Deep5hmC-diff takes the labeled DhMRs/non-DhMRs in a case–control design of 5hmC-seq as the training set to predict genome-wide DhMRs and may discover de novo DhMRs. ( D ) Model architecture of Deep5hmC. Deep5hmC consists of both sequence modality and epigenetic modality consisting of their own convolutional neural networks (CNNs) to derive separate feature representations, which will be joined later via the multi-modal factorized bilinear (MFB) pooling fusion layer. The output of the MFB fusion layer will further connect to fully connected layers and the output layer afterward.
Figure Legend Snippet: Overview of Deep5hmC. ( A ) The training set of Deep5hmC can be derived from matched 5hmC-seq and other epigenetic data such as histone ChIP-seq or DNase-seq/ATAC-seq from one condition. Specifically, the 5hmC-seq data can be collected from tissue-specific human tissues, which include bladder, brain, breast, heart, kidney, liver, lung, marrow, ovary (female), pancreas, placenta (female), prostate (male), colon (sigmoid), colon (transverse), skin, stomach, and testis (male). The matched tissue-specific epigenetic data, such as histone ChIP-seq data profiling histone modification and DNase-seq/ATAC-seq profiling chromatin accessibility, can be collected from public consortiums such as Roadmap Epigenomics and ENCODE. In this context, Deep5hmC aims to predict genome-wide 5hmC modification in a single condition. ( B ) The training set of Deep5hmC can also be derived from matched 5hmC-seq and ChIP-seq from a case–control study (e.g. Alzheimer’s disease (AD) versus healthy control) for predicting differentially hydroxymethylated regions (DhMRs). ( C ) Deep5hmC is a multimodal deep learning model to improve the prediction of tissue/cell type-specific genome-wide 5hmC modification by leveraging both DNA sequence and epigenetic features such as histone modification and chromatin accessibility. Deep5hmC consists of four modules, including Deep5hmC-binary, Deep5hmC-cont, Deep5hmC-gene, and Deep5hmC-diff. Specifically, Deep5hmC-binary takes the labeled 5hmC peaks and non-peaks as the training set to identify the 5hmC-enriched regions. Deep5hmC-cont takes the normalized read counts in 5hmC peaks and aims to predict the continuous 5hmC modification genome-wide. By leveraging Deep5hmC-cont, Deep5hmC-gene aggregates the predictions of Deep5hmC-cont in the gene bodies as the surrogate for the predicted gene expression. Different from Deep5hmC-binary, Deep5hmC-diff takes the labeled DhMRs/non-DhMRs in a case–control design of 5hmC-seq as the training set to predict genome-wide DhMRs and may discover de novo DhMRs. ( D ) Model architecture of Deep5hmC. Deep5hmC consists of both sequence modality and epigenetic modality consisting of their own convolutional neural networks (CNNs) to derive separate feature representations, which will be joined later via the multi-modal factorized bilinear (MFB) pooling fusion layer. The output of the MFB fusion layer will further connect to fully connected layers and the output layer afterward.

Techniques Used: Derivative Assay, ChIP-sequencing, Modification, Genome Wide, Control, Sequencing, Labeling, Expressing

Distribution pattern of histone modification around 5hmC peaks. EB 5hmC peaks are collected from “Forebrain Organoid” 5hmC-seq data and ChIP-seq data in “Brain Angular Gyrus” from seven histone marks are collected from Roadmap Epigenomics. Histone features are obtained and averaged in the neighborhood of all 5hmC peaks for the positive and negative sets, respectively. Specifically, histone features are created by segmenting an extended genomic region of 10 kb both upstream and downstream of each 5hmC peak into 41 1 kb windows with a sliding size of 500 bp and counting reads for each 1 kb windows. For each histone mark, the Kolmogorov–Smirnov test is performed to test the distribution difference of histone features between positive and negative 5hmC peaks and the P -value is reported.
Figure Legend Snippet: Distribution pattern of histone modification around 5hmC peaks. EB 5hmC peaks are collected from “Forebrain Organoid” 5hmC-seq data and ChIP-seq data in “Brain Angular Gyrus” from seven histone marks are collected from Roadmap Epigenomics. Histone features are obtained and averaged in the neighborhood of all 5hmC peaks for the positive and negative sets, respectively. Specifically, histone features are created by segmenting an extended genomic region of 10 kb both upstream and downstream of each 5hmC peak into 41 1 kb windows with a sliding size of 500 bp and counting reads for each 1 kb windows. For each histone mark, the Kolmogorov–Smirnov test is performed to test the distribution difference of histone features between positive and negative 5hmC peaks and the P -value is reported.

Techniques Used: Modification, ChIP-sequencing

Comparison of unimodal and multimodal Deep5hmC for predicting binary 5hmC modification sites. When using histone modification in the epigenetic modality, two unimodal models of Deep5hmC: Deep5hmC-Seq using only DNA sequence as the model input and Deep5hmC-His using only histone modification as the model input are compared to the default multimodal Deep5hmC-Seq+His using both DNA sequence and histone modification as the model input. 5hmC peaks from the EB stage “Forebrain Organoid” and two histone marks: H3K4me1 and H3K4me3 ChIP-seq data in all brain regions from Roadmap Epigenomics are used as the training set. ( A ) AUROC reported for three compared methods. ( B ) AUPRC reported three compared methods.
Figure Legend Snippet: Comparison of unimodal and multimodal Deep5hmC for predicting binary 5hmC modification sites. When using histone modification in the epigenetic modality, two unimodal models of Deep5hmC: Deep5hmC-Seq using only DNA sequence as the model input and Deep5hmC-His using only histone modification as the model input are compared to the default multimodal Deep5hmC-Seq+His using both DNA sequence and histone modification as the model input. 5hmC peaks from the EB stage “Forebrain Organoid” and two histone marks: H3K4me1 and H3K4me3 ChIP-seq data in all brain regions from Roadmap Epigenomics are used as the training set. ( A ) AUROC reported for three compared methods. ( B ) AUPRC reported three compared methods.

Techniques Used: Comparison, Modification, Sequencing, ChIP-sequencing

Related Articles

other:

Article Title: Deep5hmC: predicting genome-wide 5-hydroxymethylcytosine landscape via a multimodal deep learning model.
Article Snippet: Without loss of generality, we utilize 5hmC peaks from four developmental stages in “Forebrain Organoid” and ChIP-seq data from two histone marks: H3K4me1 and H3K4me3 collected from all brain regions in Roadmap Epigenomics (Supplementary Table S2).

Article Title: Deep5hmC: predicting genome-wide 5-hydroxymethylcytosine landscape via a multimodal deep learning model.
Article Snippet: Specifically, we choose 5hmC peaks from four developmental stages in “Forebrain Organoid” and ChIP-seq data from all brain regions of seven histone marks in Roadmap Epigenomics (Supplement Table S1) and evaluate the predictive performance for each histone mark in terms of AUROC and AUPRC.

Article Title: Identification of causal genes and mechanisms by which genetic variation mediates juvenile idiopathic arthritis susceptibility using functional genomics and CRISPR-Cas9
Article Snippet: The regulatory roles of individual SNPs identified in the most recent JIA GWAS [ ] were investigated through annotation that incorporated publicly available ChIP-seq data from the Roadmap Epigenomics Consortium [ ], EpiMap predicted immune cell related enhancers [ ], as well as in-house generated ATAC-seq peaks and PCHi-C data from the 3 JIA CD4+ T cell samples.

Article Title: Deep5hmC: predicting genome-wide 5-hydroxymethylcytosine landscape via a multimodal deep learning model.
Article Snippet: In cases where tissue-matched ChIP-seq data is unavailable at Roadmap Epigenomics, we retrieve it from ENCODE portal (Sloan et al., 2016) (https://www.encodeproject.org/).

Article Title: Different genome-wide DNA methylation patterns in CD4+ T lymphocytes and CD14+ monocytes characterize relapse and remission of multiple sclerosis: Focus on GNAS.
Article Snippet: Background: Relapsing-remitting multiple sclerosis (RRMS) is a most common form of multiple sclerosis in which periods of neurological worsening are followed by periods of clinical remission.. RRMS relapses are caused by an acute autoimmune inflammatory process, which can occur in any area of the central nervous system.. Although development of exacerbation cannot yet be accurately predicted, various external factors are known to affect its risk.

Article Title: Program of the 94 th Annual Meeting of the American Association of Biological Anthropologists.
Article Snippet: Book i PROGRAM OF THE 94TH ANNUAL MEETING OF THE AMERICAN ASSOCIATION OF BIOLOGICAL ANTHROPOLOGISTS

Functional Assay:

Article Title: Targeting aryl hydrocarbon receptor functionally restores tolerogenic dendritic cells derived from patients with multiple sclerosis
Article Snippet: .. Bars represent log-transformed binomial q values of the GO term enrichment for the HD mDCs - MS mDCs contrast. (B) Chromatin functional state enrichment analysis of the differentially hypomethylated probes in HD-MS mDC contrast, based on CD14+ primary cells ChromHMM public data from Roadmap Epigenomics Project. ..



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