The Xerox Mechanism Is An Analogous Mimic Of Our Cellular Functions.

It all has to do with the copying that goes on during cell replication.

Itwas Chester Carlson who first found a breakthrough in electrophotography back in 1938, which was eventually named “xerography”, and that’s how the term “Xerox” is so commonly equated with photocopying these days.

People who have used photocopier machines do notice that they are able to print out nearly identical copies of different documents and images, based on the work that Carlson did in those earlier years. However, a document that gets copied over and over and over again will tend to produce copies that are worse off in quality over time.

But of course, what we don’t figure out is that this copying mechanism is but an analogous mimicry of what goes on in our body — particularly in the aspect of how the cells in our body replicate.

How do the cells in our body replicate?

That, of course, is a long and boring biology topic that can span multiple videos, as is evidenced here.

But basically, what we have to do is to reproduce a copy of the deoxyribonucleic acid (DNA) identifier strands that a cell has, such that it can undergo this process known as binary fission.

This means that the DNA in the cell must undergo a copying mechanism.

The DNA in each cell exists as 2 strands that are woven together with different nucleic acids involved. One nucleic acid on one strand is bonded to another nucleic acid on another strand, and we call that bond a “base pair”. The DNA in the human genome contains approximately 3 billion of those base pairs.

During the replication process, the 2 strands must be separated from each other, and the DNA polymerase enzymes start to read each strand and synthesise a complementary strand to match the strand that is being read.

Such that we’d see the development of 2 new DNA strands at the end of the day. They can fuse up to form the DNA backbone of the new cell that is to be synthesised.

But now, given that the copying mechanism isn’t completely perfect, there will always be room for error in the reading of the original strand and the synthesis of the new strand.

What’s the problem with an imperfect copy?

Fragments of base pairs are defined as “genes”, and these genes are responsible for directing the cell to produce specific proteins and enzymes that can signal other cells to do something.

Groups of 3 base pairs are used to encode amino acids that comprise the entire protein.

When the DNA copying mechanism is off, and the amino acid encoding is off, there would be a problem for the cell to synthesise the requisite amounts of proteins that it ought to be producing in the first place.

We call that a mutation of the DNA. (Chemical reactions with DNA may also force unwanted mutations of DNA.)

That’s an issue with cell productivity right there, and that there cell ought to be culled via autophagy really quickly.

Otherwise, there is a potential problem if they do multiply, right?

When the negative effects of one employee rubs off onto their entire team, the entire team is on its way to becoming a toxic cancer to the organisation, isn’t it?

And that’s why organisations want to eliminate such toxic employees — they don’t those negative behaviours and trends to spread and permeate throughout the organisation.

That’s also why cells that aren’t producing enough of the requisite proteins ought to be culled, too. We definitely don’t want them to wreak more havoc in our body down the line, and hence we get them culled before they can spread.

So when we talk about a mutated COVID virus…

The same concept applies.

Because when we do get infected by the virus, what we will see is that the virus manages to get into a cell and reprogrammes it to only produce copies of the virus RNA/DNA strands.

These virus copies can then proceed to infect other healthy cells and amplify the effects of virus multiplication exponentially.

And that’s the part of the infection process that we don’t want to reach, ever.

Because when there’s that exponential multiplication of all these virus-infected cells, the defensive workload of the immune system also has to increase likewise.

Our bodies would be at war against the viral invaders.

In World War 2, there were frequent bombings, airstrikes, air raid sirens, and all that going on in Europe.

A similar event would be happening in our bodies during an infection — we term that as inflammation, and that’s when the immune cells are actually producing much more pro-inflammatory cytokines as a response to the viral invasion.

Same thing for when one nation is dropping bombs on another, isn’t it?

We don’t want that happening in real life — but neither do we want that happening to ourselves.

Now, this virus contains a ribonucleic acid (RNA) identifier. RNA is a single-stranded nucleic acid identifier, which is different from the double-stranded DNA identifier that our cells have.

But they’re all made up of nucleic acids and can be reproduced via the same copying methods. Therefore…

Could the RNA identifier on this virus become mutated over time, too?

Of course, it can!

And can that not form the more infective Delta variant of the COVID-19 virus that is currently a hot topic for discussion at the moment?

Further implications of imperfect copying.

While we’re just looking at all these different base pairs out there, and figuring out that they’re mainly used as genes to synthesise essential proteins…

Proteins themselves are complex biomolecules. They can comprise up to 20 different types of amino acids in long chains.

And as we know it, long chains do tend to tangle up over time as they seek a most stable configuration (try looking at unsecured wires that knot themselves up over time).

Some of these amino acids prefer the company of other similar amino acids and dislike other amino acids, hence the protein will fold and contort in ways for it to achieve the most stable configuration as well.

If we were to encode the wrong amino acids into the protein sequence, the folding configuration will be changed.

It’s usually for the worse, not the better.

A mutation in the methylenetetrahydrofolate reductase (MTHFR) gene, for instance, results in the production of an MTHFR enzyme that isn’t all that good in converting homocysteine back to methionine.

And too much homocysteine in the blood may not necessarily be good.

Sometimes we’re born with it already… but sometimes we get it from faulty copying mechanisms.

Unfortunately, the first stage of copying in our bodies comes from the DNA that our father’s sperm and our mother’s egg cells provide.

When that is copied erroneously, we can see various birth defects. People born with autoimmune conditions, for instance.

It’s hereditary.

But of course, our own copying mechanisms can go bad over time.

The quality checkers may not be doing their jobs.

During the cell replication cycle, there is the G1/S checkpoint that prevents a cell from commencing DNA synthesis if too many faults are found.

But if the G1/S ain’t doing their job and allowing the faulty copies to go through…

Imagine if one’s body allowed the faulty replication of the mutated COVID-19 Delta variant… and the infected cells that are hypnotised by the virus are just mindlessly producing more and more new copies of the Delta variant?

They’d be highly infectious people. They can’t blame our parents for that, can they?

Unfortunately, as imperfect photocopying mechanisms are…

The copying mechanisms in our body are no better — they will still be prone to errors.

But the million-dollar question is: can we catch them and dispose of the faulty replicates quickly and efficiently enough before they actually become a problem?

Chester Carlson would have been proud of his xerography invention, though. Its reliability at producing good-quality copies of printed documents is still pretty high!

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