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Issue 5 Article 6

Epigenetic Modifications: The Invisible Architects of Cellular Fate

25/5/20

By:

Liu Yu An

Edited:

Crystal Tay Yuan Ying

Tag:

Molecular Biology and Biochemistry

Ever wondered how your body pulls off the wild trick of making brain cells, skin cells, liver cells — all completely different, with different structures and functions— using the exact same DNA? It’s not like each cell has a different version of your genome. They’re all reading from the same book. The difference? They’re flipping to different pages. That’s where epigenetics comes in — the behind-the-scenes system that decides which parts of your DNA get read and which stay closed like forgotten chapters.


This isn’t science fiction or some fringe theory. It’s real, and it’s constantly happening in your body. While the DNA stays the same, epigenetic modifications — tiny chemical tags and tweaks — control which genes get turned on or off. So even though your muscle cells and nerve cells start from the same instructions, epigenetics helps each one become the specialist it needs to be.


What’s Actually Going On?

Let’s break it down. Epigenetics works through a few main tools: DNA methylation, histone modifications, and non-coding RNAs. Don’t worry — that might sound heavy, but the basic idea is pretty simple: these are ways of packaging and managing DNA so that only the right bits are used at the right time.


Take DNA methylation — this is like putting a sticky note on a gene that says “do not open.” Methyl groups attach to certain spots on the DNA (mostly cytosine bases), and when they do, the gene usually gets shut down. It’s one way your cells avoid turning on every gene all the time. That would cause chaos.


Then there’s histone modification. Picture your DNA wrapped around little protein spools — those are histones. Depending on how those spools get modified (by acetylation or methylation, for example), the DNA can be more tightly wound (harder to read) or more relaxed (easier to read). It’s like tightening or loosening the cap on a marker — sometimes you want it sharp, sometimes you want it muted.


And finally, we have non-coding RNAs. These don’t make proteins like the usual RNAs you hear about, but they’re far from useless. They help regulate gene expression, sometimes by blocking certain messages or guiding protein machinery to the right spots on the genome.


Why Does This Matter?

One place where epigenetics really shines is in stem cells — the ultimate blank slates. These cells can turn into pretty much any type of cell in the body. The way they figure out what to become is through a whole series of epigenetic changes. It’s like the cell slowly narrowing down its career options until it finally settles on a job — heart cell, skin cell, neuron, you name it.


Even cooler, scientists have figured out how to reverse this process. You can take a regular adult cell — say, from your skin — and rewind its epigenetic programming to turn it back into a stem-cell-like state. These are called induced pluripotent stem cells (iPSCs), and they’re opening up amazing possibilities in regenerative medicine. Imagine growing replacement tissues or organs from your own cells — no rejection risk, no donor needed.


When Things Go Sideways

Of course, if epigenetics can help things run smoothly, it can also mess things up. When these systems break down, the consequences can be serious. One example: in some cancers, certain genes that normally stop tumors from growing get epigenetically silenced. No mutation needed — just the wrong epigenetic tags in the wrong place.


In fact, researchers have found links between faulty epigenetic processes and all kinds of diseases — from leukemia to Alzheimer’s. That’s why epigenetic therapy is a growing field. Drugs that target these processes — like histone deacetylase inhibitors or DNA methylation blockers — are being used to try and reset the system, turning the right genes back on or off.


And we’re still just scratching the surface. The hope is that by better understanding these invisible instructions layered on top of our DNA, we’ll be able to treat disease in a much more precise, personalized way.


So What’s the Big Picture?

Epigenetics doesn’t change your genes — it changes how your genes are used. It’s a bit like having a huge cookbook and only ever making a few recipes. The book stays the same, but the tabs and bookmarks — the ones telling you what to cook tonight — are what really guide the action.


And those bookmarks? They’re not permanent. They can change based on what you eat, how much you sleep, whether you're stressed, even what chemicals you're exposed to. In a way, epigenetics is the biological bridge between your environment and your genes.


We’re still learning how to read and rewrite this hidden layer of information. But the more we understand it, the more we realize:we’re not just at the mercy of our DNA — we’re also shaped by these subtle, powerful edits that are happening all the time.


References

  1. Abrajano, J. J., Qureshi, I. A., & Mehler, M. F. (2012). Developmental and functional epigenomics of neural progenitor cells. Neuroscience, 248, 512-532.

  2. Bartel, D. P. (2004). MicroRNAs: genomics, biogenesis, mechanism, and function. Cell, 116(2), 281-297.

  3. Guttman, M., & Rinn, J. L. (2012). Modular regulatory principles of large non-coding RNAs. Nature, 482(7385), 339–346.

  4. Jones, P. A., & Baylin, S. B. (2007). The epigenomics of cancer. Cell, 128(4), 683-692.

  5. Kouzarides, T. (2007). Chromatin modifications and their function. Cell, 128(4), 693-705.

  6. Ley, T. J., Ding, L., & Cancer Genome Atlas Research Network (2010). DNMT3A mutations in acute myeloid leukemia. New England Journal of Medicine, 363(25), 2424-2433.

  7. Takahashi, K., & Yamanaka, S. (2006). Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell, 126(4), 663-676.

  8. Qureshi, I. A., & Mehler, M. F. (2010). Epigenetic mechanisms underlying human epileptic disorders and the process of epileptogenesis. Neurobiology of Disease, 39(1), 53-60. PMID: 19804829

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