epigenetic modification
Definition
Epigenetic modifications are heritable chemical changes to DNA or histone proteins that alter gene expression without changing the underlying DNA sequence. These modifications include DNA methylation, histone acetylation, methylation, phosphorylation, and ubiquitination. They regulate chromatin structure and accessibility, controlling which genes are active or silenced in specific cell types and conditions. Epigenetic modifications are crucial for normal development, cellular differentiation, and genomic imprinting, but aberrant patterns are implicated in cancer, neurological disorders, and metabolic diseases. Unlike genetic mutations, epigenetic changes are potentially reversible, making them attractive therapeutic targets. Environmental factors, aging, and lifestyle can influence epigenetic patterns, creating a dynamic interface between genotype and phenotype.
Visualize epigenetic modification in Nodes Bio
Researchers can visualize epigenetic modification networks by connecting modified genomic regions to target genes, transcription factors, and downstream pathways. Network graphs can reveal how methylation patterns at CpG islands correlate with gene expression changes, or how histone modifications cluster around regulatory elements. Users can integrate ChIP-seq and bisulfite sequencing data to map modification landscapes and identify epigenetic regulatory hubs controlling disease phenotypes or developmental processes.
Visualization Ideas:
- Epigenetic modification-to-gene regulatory networks showing which modifications control specific gene clusters
- Multi-layer networks connecting DNA methylation sites, histone marks, and transcription factor binding events
- Temporal networks tracking epigenetic changes across cell differentiation or disease progression stages
Example Use Case
A cancer research team investigating tumor suppressor gene silencing in colorectal cancer uses genome-wide methylation data to identify hypermethylated promoter regions. They map these methylation sites to affected genes and their protein products, revealing a network where aberrant DNA methylation at specific CpG islands silences multiple DNA repair genes simultaneously. By visualizing the connections between methylated regions, silenced genes, and disrupted repair pathways, they identify potential epigenetic biomarkers and prioritize demethylating agents that could reactivate tumor suppressor function across multiple nodes in the network.