A Kaleidoscopic Genome: The Science Behind Homo Nova

What if it was possible to wilfully alter the expression of our DNA? Ulrik Magnusson, our protagonist in the story of Homo Nova is the only known person in the world who has a kaleidoscopic genome: a condition in which his genome undergoes hyper- and hypomethylation—the switching on and off of genes. Sound like science fiction? Read on, and you may find the truth surprises you…so, stick with it, okay?

So what’s a kaleidoscopic genome? Well, imagine you’re looking down into a kaleidoscope, where you see a mosaic of vibrant colours. Then, when you twist the lens, countless arrangements of unique patterns play out despite all the original components remaining the same. Our genome, or rather our DNA operates much like that. At first, we observe the static mosaic of our genetics, that is, all our visible traits (phenotype); but when the environmental conditions are altered, our genome has the ability to undergo fantastical permutations, arranging and expressing itself in different ways, yet all the while its core components (genotype) remain the same.

Like a kaleidoscope, DNA isn’t a static picture. It can be altered and expressed in different ways to manifest varied visible characteristics.

Like a kaleidoscope, DNA isn’t a static picture. It can be altered and expressed in different ways to manifest visible variation in characteristics. And by the way, this isn’t some far-fetched fantasy about humans metamorphosing into hybrid creatures or mutants. It’s about real, demonstrable variation, and there is a plethora of peer-reviewed literature out there on epigenetics for further reading on the subject.

Let’s dive headfirst into an example with monozygotic twins (identical). Think about this for a moment: how is it that identical twins can exhibit different traits? Twins—born with the exact same DNA sequence. Shouldn’t twins exhibit the exact same observable characteristics, all the time? So why, for example, in instances where one identical twin develops schizophrenia, is there only a ~50% chance the other twin will develop it? Why wouldn’t the other twin always develop the condition? Why not 100% of the time? Discordance like this is often dismissed as an environmental factor, but environment is only the tip of the iceberg. To cite another famous example, in the agouti mice experiment (pictured), all the mice are genetic clones, yet some have yellow fur, some are tawny, and others are shades in between. Or take, for example, queen bees and worker bees; they’re genetically identical, but why are they completely different in form and function? Again, environment has its part to play in variation, but the conditions of a laboratory and a beehive are pretty standardised. So, we need to look under a microscope at the cellular level in order to understand what’s happening. And it’s in doing so, we begin to unravel the mystery of methylation.

So, what exactly is methylation? Well, it’s a process in which methyl groups bind to genes and instruct them. They do this by reading and interpreting the language of DNA within our cells. Think of methylation as a sort of master switch. Methylation can change the activity or expression of DNA without changing (mutating) the DNA itself, and it does this by switching genes on and off. The degree of methylation within DNA is the defining factor in those examples of variation cited above in twins, bees, and mice.

Now, here’s the bigger picture: we each of us have within our genome around 20,000 genes (the exome) which encode for proteins—which perform all kinds of functions like repairing, growing, and regulating our bodies. 20,000 may sound like a lot of genes, but the exome accounts for a paltry 2% of our total genome. Why, then, do we possess so much junk DNA (non-coding DNA) when so little of it is readable or useful? Well, maybe the remaining 98% isn’t excess baggage that has no biological function as once supposed, but maybe it’s untapped potential.

But where did it come from, this alleged ‘junk DNA’? And why is it piggybacking onto our genetic barcode? Well, every person (or organism) inherits all their DNA from two parents, as they did from theirs, and so forth. Go back far enough, and you’ll see a whole legacy of DNA has been passed down from our ancestors from one generation to the next. It’s a signature that stems back to a point in history around 3.5 billion years ago when life emerged on earth as single-celled organisms. So, perhaps the remaining 98% of the genome is an archive of ancestral genes and are the traces of ancient DNA which have been passed down from our primordial ancestors. Not just human ancestors but non-human, too…

Our genome is like a supercomputer where the exome (the functional 2%) is the latest software operating system that’s currently in use, and the remaining 98% is an archive or memory of files we’ve inherited from our ancestors.

Think of our genome as a supercomputer, where the exome (the functional 2% of genes) is the latest software operating system that’s currently in use, and the remaining 98% is an archive or memory of backup files we’ve inherited from our ancestors. At present, those ancestral files aren’t currently in use. They’ve become redundant, inactive, dormant, because they no longer serve a survival advantage in our modern world, so our bodies no longer carry out the transcription of these genes, and so they’re left switched off. But are these files still accessible? Is it possible to switch on ancestral genes? Examples in nature are proof of that.

We see rare occasions of dormant genes being awoken from their slumber. Humans born with vestigial tails, webbed feet, scaly skin, hairy complexions, and the like. Even 150 years before the discovery of DNA and epigenetics, Charles Darwin himself wrote at length about genetic reversion when he observed reversion in feral pigeons which had appearances similar to that of the rock pigeon. Reversion being the phenomenon that a trait of remote ancestors can reappear in organisms whose more immediate ancestors lack the trait.

Modern science has made rapid gains since then, and we now have an abundance of evidence demonstrating that methylation is the magic stimulus for such radical reversion and genome expression. But what the limits of methylation are, nobody knows; and what this could mean for Ulrik Magnusson, our protagonist who has a kaleidoscopic genome and can switch on ancestral genes, nobody would ever suppose…

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