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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Spreading of Chromatin Modifications02:25

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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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Chromatin Structure Regulates pre-mRNA Processing02:41

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In eukaryotic cells, nascent mRNA transcripts need to undergo many post-transcriptional modifications to reach the cell cytoplasm and translate into functional proteins. For a long time, transcription and pre-mRNA processing were considered two independent events that occur sequentially in the cell. However, it has now been well established that transcription and pre-mRNA processing are two simultaneous processes that are precisely regulated inside the cell.
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Human Genetics01:28

Human Genetics

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Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
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What is Gene Expression?01:36

What is Gene Expression?

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A gene is a stretch of DNA that serves as the blueprint for functional RNAs and proteins. Since DNA is comprised  of nucleotides and proteins are comprised of amino acids, a mediator is required to convert the information encoded in DNA into proteins. This mediator is the messenger RNA (mRNA). mRNA copies the blueprint from DNA by a process called transcription. In eukaryotes, transcription occurs in the nucleus by complementary base-pairing with the DNA template. The mRNA is then...
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Related Experiment Video

Updated: Jun 21, 2025

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
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Crosstalk between epitranscriptomic and epigenomic modifications and its implication in human diseases.

Chengyu Li1, Kexuan Chen1, Qianchen Fang1

  • 1The Second Affiliated Hospital & Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou 311121, China; State Key Laboratory of Transvascular Implantation Devices, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 311121, China.

Cell Genomics
|July 9, 2024
PubMed
Summary

This study maps the directional crosstalk between N6-methyladenosine (m6A) and epigenomes like DNA methylation (DNAme) and H3K27ac. These regulatory pathways are linked to complex human diseases, offering new insights into disease mechanisms.

Keywords:
DNA methylationGTExGWASH3K27acMendelian randomizationcolocalizationm(6)A crosstalk

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Area of Science:

  • Epigenetics and Molecular Biology
  • Genomics and Computational Biology

Background:

  • N6-methyladenosine (m6A) modification plays a key role in gene regulation, but its interplay with other epigenomic marks and its disease relevance are not fully understood.
  • Understanding the directionality of crosstalk between m6A and epigenomes like DNA methylation (DNAme) and H3K27ac is crucial for deciphering gene regulatory networks.

Purpose of the Study:

  • To create directional maps of the crosstalk between m6A and DNAme/H3K27ac using quantitative trait loci (QTLs).
  • To investigate the association of these m6A-epigenome regulatory pathways with complex human diseases.

Main Methods:

  • Utilized quantitative trait loci (QTLs) as genetic instruments to infer causal relationships.
  • Delineated directional regulatory loci for m6A-to-DNAme, m6A-to-H3K27ac, DNAme-to-m6A, and H3K27ac-to-m6A.
  • Integrated identified regulatory loci with genome-wide association study (GWAS) data for various complex diseases.

Main Results:

  • Identified a significant number of directional regulatory loci, including 4,733 m6A-to-DNAme and 61,775 DNAme-to-m6A loci.
  • Observed distinct genomic location preferences for different regulatory directions.
  • Prioritized thousands of genetic variants associated with complex diseases like neuroticism, depression, asthma, and coronary artery disease through these crosstalk maps.

Conclusions:

  • Established directional regulatory paths between m6A and epigenomic layers, providing insights into locus-specific crosstalk.
  • Uncovered novel regulatory circuits underlying human diseases by linking m6A-epigenome interactions to disease-associated GWAS loci.
  • Demonstrated the utility of QTL-based mapping for dissecting complex epigenetic regulatory networks and their role in disease pathogenesis.