This model demonstrates how DNA methylation, histone acetylation and H3K4 methylation combine to set chromatin compaction and, in turn, the expression level of four real human genes — BRCA1, TP53, MYC and CDKN2A. Silencing and activating scores are weighted and summed to give each gene an expression probability between 0 and 1, whilst an inheritance probability estimates the likelihood that the current epigenetic state would persist through cell division.
Four sliders drive a weighted silencing-versus-activation formula per gene. Methylated CpG sites and tight chromatin compaction push expression down; histone acetylation and H3K4 methylation push it up. An environmental signal adds a per-gene boost or penalty on top.
Drag the CpG methylation, histone acetylation, H3K4 methylation and chromatin compaction sliders, then choose an environmental signal (heat, cold, nutrient-rich or starvation) from the dropdown. Watch the nucleosome view and the four-gene expression bar chart update instantly, alongside overall expression, inheritance probability and chromatin state readouts.
Roughly 60-70% of human gene promoters sit within CpG islands, and methylating these islands is one of the commonest ways tumour suppressor genes such as TP53 are silenced in cancer.
Four real human genes: BRCA1, TP53, MYC and CDKN2A. Each has its own expression bar and responds differently to the same methylation, acetylation and compaction settings because environmental signals apply a distinct boost or penalty to each gene.
Silencing factors (methylation weighted highest, then compaction, then low H3K4) are combined and subtracted from activating factors (acetylation, H3K4 methylation and any environmental boost), then clamped between 0% and 100% to give the bar height for each gene.
It combines acetylation, unmethylated CpG fraction and H3K4 methylation into a single score approximating how likely the current active or silenced state is to be copied faithfully onto daughter cells after division.
The chromatin state readout checks compaction and acetylation together with methylation: high compaction above 70% gives heterochromatin, high acetylation with low methylation gives euchromatin, and everything else is labelled mixed.
Heat stress, cold stress, nutrient-rich and starvation each apply a fixed positive or negative boost to each of the four genes' activation score before the expression bars are redrawn, mimicking how real environmental cues can shift gene expression through epigenetic channels.
Epigenetics refers to heritable changes in gene expression that occur without altering the underlying DNA sequence. The two most studied mechanisms are DNA methylation—the addition of methyl groups to cytosine bases at CpG sites, typically silencing nearby genes—and histone modification, including acetylation and deacetylation of the histone proteins around which DNA is wound. These chemical marks form an epigenetic code that cells read to determine which genes are active.
Histone acetylation, added by histone acetyltransferases (HATs), loosens the chromatin structure, making DNA accessible to transcription factors and RNA polymerase, thus activating gene expression. Histone deacetylases (HDACs) remove acetyl groups, compacting chromatin and silencing genes. Methylation of histone H3 at lysine 4 (H3K4me3) marks active promoters, while H3K27me3 marks repressed regions. These marks are written, read, and erased by specific enzyme families.
This simulator visualizes how methyl and acetyl marks accumulate on a gene's regulatory region and how they affect the probability of transcription. You can observe bistable states—where a gene is stably on or off—and how environmental signals can flip the epigenetic switch. Epigenetic dysregulation underlies cancers, developmental disorders, and aging, making it a major target for drug discovery.
How is epigenetics different from genetics?
Genetics concerns changes in the DNA sequence itself—mutations, insertions, deletions. Epigenetics involves chemical modifications to DNA or its associated proteins that change which genes are expressed without changing the sequence. Epigenetic changes are often reversible and can be influenced by diet, stress, toxins, and age, whereas most DNA sequence mutations are permanent.
Can epigenetic changes be inherited by children?
In most cases, epigenetic marks are erased and reset during the formation of egg and sperm cells (epigenetic reprogramming). However, some marks escape this erasure and are transmitted to offspring—a phenomenon called transgenerational epigenetic inheritance. Evidence in plants is strong; in mammals it has been demonstrated in specific circumstances, such as the effects of famine or certain toxin exposures on multiple generations.
What is chromatin remodeling and why does it matter?
Chromatin remodeling is the repositioning or restructuring of nucleosomes (DNA-histone complexes) to control DNA accessibility. When chromatin is loosely packed (euchromatin), transcription factors can bind and genes are expressed. Tightly packed heterochromatin blocks access, silencing genes. Chromatin remodeling complexes use ATP hydrolysis to slide, eject, or restructure nucleosomes, making it one of the primary mechanisms for regulating developmental gene expression programs.
Cancer cells frequently show global DNA hypomethylation (reactivating oncogenes and transposable elements) combined with focal hypermethylation at tumor suppressor gene promoters, silencing critical growth-control pathways. HDAC inhibitors and DNA methyltransferase inhibitors are approved cancer drugs that attempt to reverse these aberrant epigenetic states, reactivating silenced tumor suppressors. The reversibility of epigenetic marks makes them attractive therapeutic targets compared to irreversible DNA mutations.
CpG islands are genomic regions of roughly 200–2000 base pairs with a higher-than-expected frequency of CpG dinucleotides. About 60–70% of human gene promoters contain CpG islands. When unmethylated, they are associated with active or poised promoters. Methylation of CpG islands at tumor suppressor gene promoters is one of the most common epigenetic events in cancer. They are widely used as biomarkers for cancer detection and prognosis in liquid biopsy assays.