Logan Collins – TRANSCRIPT
Antibiotic resistance is an extremely serious threat in today’s world. It costs the US healthcare system over 20 billion dollars per year. And it kills an estimated 23,000 people per year in the US alone. In addition, there are concerns that antibiotic resistance might result in something far worse. It may result in something along the lines of the bubonic plague, which killed approximately a third of Europe’s population of the time that it occurred. We, of course, don’t want this.
So what’s being done about this? Well, traditional antibiotics tend to use compounds which will fit into the molecular machines that run bacteria, the macromolecules, those large molecules, that help to make bacteria work. And what they do is they’ll fit into a particular crevice as a key fits into a lock. And the antibiotics will inactivate these macromolecules and disrupt their function, thus killing off the bacteria. However, when bacteria in the population have variations of these molecules, which are differently shaped, the antibiotic key can no longer fit into the large molecular lock. And thus, the bacteria gains resistance.
Then these bacteria propagate in population, and it results in an antibiotic resistance population of bacteria. There are also some other ways that antibiotic resistance arises, including antibiotics not being able to enter the cell, antibiotics being pumped out of the cell, and enzymes which will chop up the antibiotics. I’ve been conducting research at the University of Colorado, Boulder, at the Chatterjee Lab, and thus far, I’ve gotten some very encouraging results, and I’m excitedly continuing to pursue the next steps in my research.
So what have I been doing? I have created an artificial gene that codes for antimicrobial polypeptides. This artificial gene is — Well, let me first explain what that means. Basically, I created a gene that is capable of synthesizing misfolded proteins upon entering into the bacterial cell. These misfolded proteins disrupt the biochemical balance in the bacterial cell by causing chaos through aggregation.
And I’ll get back to that in just a moment. As you can see, this causes a widespread disruption in the bacteria, rather than targeting a specific molecule. And because of this, it’s got great promise in being more effective than traditional antibiotics because the bacteria won’t be able to simply change the shape of one molecule. They will have to undergo a system’s wide adaptation if they are to gain resistance.