Epigenetics

Epigenetics in a Minute

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• published: 20 Mar 2015
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Once upon a time in the world of genetics, two identical twins were born. The two baby boys were named Jim and Tim Van Horn. All observable phenotypes were alike, this was no surprise because they were genetic clones. Their hair, eyes, behaviours were the same– including all their milestones. My oh my , they were definitely twin brothers!! Then one day their worlds changed when mommy and daddy stopped loving each other. No longer wanted to be husband and wife, moved to two different cities and started a new life. Tim lived with mom and Jim lived with dad. Different environments, different experiences for both of the lads. As time went on, the most unfortunate thing happened. They contracted different illnesses, both hospitalized and saddened. But how was this possible? They were identical you know, same genotype means same phenotypes no? What was this phenomenon that caused this alteration? Epigenetics was the reason, specifically, methylation! Tim and Jim differ epigenetically but have the identical DNA. What is this epigenetics I keep on speaking of you might say? All the cells in our bodies have the same DNA but necessarily don’t know how to behave Epigenetics provides instructions so the cells know what to do, for example, they’ll follow the muscle cell lineage and will be a muscle cell slave These instructions are provided through a chemical reaction known as methylation. Carbon and hydrogen form methyl groups, this small molecule is all that’s needed for these alterations Methylation is the covalent addition of methyl groups to DNA or histone protein, governing and directing dna transcription like a university dean Specifically methyl groups target CpG islands, attaching to a cytosine residue This stuff is fascinating, I know you’re excited too (tone change) Methylation can silence the gene by hiding the promoter sequence Preventing the binding of the RNa polymerase and eliminating transcription frequence It can also cause overexpression of a certain gene, leading to a phenotype that shouldn’t be seen Cancers and obesity just to name a few, these endless epigenetics issues can even affect you Now let’s see what happened to Jim who suffers from esophageal cancer. How is methylation going to provide the answer? The FHIT gene prevents over proliferation of epithelium cells. But since Jim was a smoker, the nicotine in his system induced FHIT methylation spells. Epithelial cells were no longer under control, always being rowdy and continuously on the roll. The cancer grew unrestricted, nothing to stop the esophagus from being constricted. Moving onto Tim, let’s talk about what happened to him Eating a nutrient poor diet, lead him on an obesity riot. Lack of methyl groups from hamburgers, fries, and shakes was certain, Resulting in the overexpression of obesity-linked genes known as TNF-Alpha and Leptin So you see that Jim and Tim had methylation differences induced by environmental factors, we can say genetics no longer was the main actor. Even though clones are the same genotypically, methylation can make them look different phenotypically (banana example) I hope you understood Epigentics my friend because this is the part where I say THE END.