The enzyme that tells aging to go f**k itself

Screw getting old. I’m at a time where I’m on the cusp of some rather grown-up life events. I get married in 6 months. Mere weeks after that, I leave graduate school and enter the job market. In protest of maturity, I thought I’d dedicate an article to some biochemical wizardry that slows down all the harmful shit you do to yourself as you age.

Just to remind you, DNA is a rather pretty-looking double-helical molecule contained in each of your body’s cells that encodes all the information they need to carry out their jobs. The two strands are made of little compounds, called bases, which act as a set of instructions for the assembly of proteins. Turning sequences of these bases into proteins is damn complicated, but know that a number of mistakes can happen in the process that alter the conversion of gene to protein, screwing with the function and health of the cell.

DNA protects itself in a few important ways. First, our cells have methods of preventing errors in DNA code, or mutations, get turned into proteins. There’s a complex set of enzymes, molecules that expedites chemical interactions, that act as a DNA proofreading system, clipping out mismatches between strands or errors encoded within one of them.

Second, DNA doesn’t sit unwrapped and unprotected in your cells; proteins called histones coil DNA and attach to other histones like a giant kaleidoscope of hugs. I could use a good hug. Aggregates of DNA hugs form singular bodies, called chromosomes, which act to preserve its contents and selectively turn on or off different segments of the strand.

DNA is wrapped around proteins called histones which are then condensed into chromosomes. Of course, you’d know this already if you’ve been reading. I’m not sure why I bother to make captions.

Lastly, DNA recruits enzymes called border patrol enzymes that check each gene’s passport and search for contraband. Mistakes still happen, but it’s the illusion of safety and security that counts.

Border enzymes

When each of your cells divides, it has to copy your entire genome, repackage it all into chromosomes, and split up the chromosomes in the right amounts to each daughter cell. You may remember the name of this from middle school biology class. You know, it’s only a little process called photosynthesis. Jeez, get with it, people.

What sucks is that this process isn’t perfect; each time a cell divides, a little bit of DNA on each end can’t be replicated and is disregarded. Because cells divide a lot, you can imagine that this gradual genetic snipping will eventually start screwing around with some damn important genes. Some of these genes may encode proteins that allow your cells to grow, reproduce, or function, and their loss would be devastating.

Our DNA knows what the hell is up though. At the tips of each chromosome are regions called telomeres, long strings of basically non-sense genetic code that is completely dispensable. These telomeres get clipped into nothingness over enough replications, and our important genetic material begins to become lost.

So yeah, here’s a chromosome with some admittedly wimpy-ass telomeres. Come on, guys, three replications and you call it quits?!

At that point, some shit starts to go down. The cells stop growing, can’t divide, or kill themselves. It is at this point that the human body begins to age; skin loses elasticity, muscles atrophy, cognitive function lessens, bones become brittle, and golf starts to sound like fun. Cells may also divide uncontrollably, a condition you may have heard of. People are doing fun runs for it all the time. You may have even had a loved one affected by it. You know, it’s a little disease that goes by the name of viral or bacterial meningitis. Come on, guys.

In 2009, Drs. Elizabeth Blackburn, Carol Greider, and Jack Szostak shared the Nobel Prize in Physiology or Medicine. According to the official Nobel announcement, “They  solved  a  long-standing  fundamental problem  in  biology;  how  can  the  ends  of  chromosomes  be  maintained  and  spared  from erosion  or  rearrangement  during  repeated  cellular  divisions?”

Not only did this trio advance what we know about the protective role of telomeres, but they also discovered a friggin awesome enzyme known as telomerase. As telomeres shorten over time, telomerase can become activated to elongate the shortening ends. Every cell in our bodies has the machinery to manufacture telomerase, though it’s usually inactive even as telomeres are damaged or shortened.

Look at telomerase getting all cozy with that primer. Just delightful.

In my opinion, determining how to activate telomerase and impede the effects of aging is currently among our most important scientific problems. Some researchers and companies are searching for answers. In fact, products are already on the market that claim to assist in the activation of telomerase. A lot of questions still remain:

1) Is it possible to not just inhibit but reverse the effects of aging by activating telomerase?
2) Could we develop a method of recovering lost genetic material?
3) What effects would extended human age have on quality of life, natural resources, and ecosystem health?
4) Does this mean Bill Cosby will never die?
5) I can’t think of any more questions.

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