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Move beyond single-layer contact maps with our Hybrid 3D Genome & Epigenome Profiling Services. Whether you need to resolve the relationship between DNA methylation and 3D folding via Methyl-Hi-C, or map interactions and accessibility simultaneously with HiCAR, we provide the dual-modality tools necessary for high-dimensional biology. Unify your epigenetic data to reveal the mechanisms of complex gene regulation. RUO.
The physical organization of the genome does not exist in isolation. It is part of a complex, high-dimensional regulatory landscape where 3D chromatin loops, DNA methylation patterns, and chromatin accessibility states constantly influence one another. Traditional methods analyze these layers separately, often losing the critical "biological crosstalk" that occurs within the same nucleus.
Our Hybrid 3D Genome & Epigenome Profiling Services are designed to break these silos. By utilizing advanced dual-modality 3D genomics technologies, we enable the simultaneous detection of chromatin architecture alongside other epigenetic markers from a single library. This "co-assay" approach ensures that the structural data you receive is perfectly aligned with the biochemical state of the DNA, providing a synergistic view of the genome that single-modality assays simply cannot capture. By integrating structural and epigenetic data, we empower researchers to identify the molecular drivers of chromatin folding and resolve the high-dimensional logic of gene regulation.
DNA methylation is a primary driver of chromatin compartmentalization and CTCF-mediated looping. Methylation at binding sites can inhibit the binding of architectural proteins, fundamentally altering 3D structure. Our services allow you to map these two layers together to reveal the methylome's direct role in 3D folding.
Methyl-Hi-C is a breakthrough technology that simultaneously captures genome-wide 3D chromatin interactions and DNA methylomes. By combining Hi-C ligation with bisulfite conversion, this method allows researchers to study how differential methylation at enhancers and insulators directly influences long-range interactions.
Linking the physical "shape" of the genome to the "openness" of its regulatory elements is essential for understanding cell-type-specific gene expression. These hybrid assays identify which "open" enhancers are physically contacting their target promoters.
HiCAR (Hi-C Accessibility Research) is a high-sensitivity co-assay that maps 3D interactions and chromatin accessibility (similar to ATAC-seq) simultaneously. It utilizes an optimized Tn5 transposition step within the Hi-C workflow to enrich for interactions at open chromatin sites.
SCA-seq (Single-molecule Chromatin Accessibility sequencing) uses long-read sequencing platforms (e.g., Nanopore) to resolve accessibility and 3D proximity on single DNA fibers. This allows for the detection of high-order, multi-way contacts.
The "neighborhood" in which a gene resides—whether at the nuclear periphery or near a speckle—is a major determinant of its transcriptional activity. Radial positioning defines the functional compartments of the nucleus.
pA-DamID (protein A-mediated DNA adenine methyltransferase identification) maps genome-wide interactions between chromatin and specific nuclear landmarks, such as the nuclear lamina. It is the premier tool for identifying Lamina-Associated Domains (LADs).
TSA-Seq (Tyramide Signal Amplification Sequencing) acts as a "cytological ruler." It measures the physical distance of genomic loci from specific nuclear compartments, such as nuclear speckles or the nuclear lamina.
Executing a hybrid 3D omics assay requires precision chemistry to ensure that the detection of the second modality (e.g., methylation) does not compromise the recovery of the 3D interaction signal.
Hybrid 3D omics services are transformative across various fields of biological inquiry, providing answers that single-modality assays cannot reach.
Track how changes in DNA methylation at lineage-specific enhancers occur simultaneously with the formation of new promoter-enhancer loops during differentiation.
Understand how aberrant methylation patterns in tumors contribute to the "rewiring" of the 3D genome, potentially activating oncogenes.
Map the radial positioning of neuronal genes and correlate their expression with 3D structural changes in the aging or diseased brain.
Study how 3D structural information and epigenetic marks are co-transmitted through the cell cycle or across generations.
While hybrid assays provide simultaneous detection, many projects require the integration of multiple independent datasets (e.g., Hi-C + ChIP-seq + RNA-seq).
For comprehensive data merging and high-dimensional visualization, explore our specialized 3D Genomics Multi-omics Integration service. We provide advanced bioinformatic pipelines to unify disparate "omics" layers into a single, navigable regulatory model.
| Research Interest | Primary Technology | Combined Data Layer | Key Insight Generated |
|---|---|---|---|
| Gene Silencing / Imprinting | Methyl-Hi-C | 3D Contacts + DNA Methylation | How methylation dictates TAD and Loop boundaries. |
| Active Regulation | HiCAR | 3D Contacts + Accessibility | Linking active enhancers to their target promoters. |
| Multi-way Contacts | SCA-seq | High-order interactions + Accessibility | Resolving complex structural "hubs" on single molecules. |
| Spatial Positioning | pA-DamID / TSA-seq | 3D Contacts + Nuclear Landmarks | Distance from nuclear lamina or nuclear speckles. |
Disclaimer: This service is for Research Use Only (RUO) and is not intended for use in clinical diagnostic or therapeutic procedures.
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