Crush it! Hey everybody, Dr. O here. In this video we’re gonna to talk about the Bacterial Ribosome and I’m just gonna add a few little nuggets I think you’ll find interesting as well. So, here we see the prokaryotic or bacterial ribosome. As you can see here it is made of a large subunit, and a small subunit just like your human ribosomes are. Uh, it happens to be the 50-S large subunit and the 30-S small subunit. Remember, the S stands for Svedberg Unit. This has to do with how they’re—how quickly they’ll centrifuge, so, don’t worry about it and as you can see,they’re not additives, so, 50 plus 30 somehow equals 70, right? But the-you should definitely know that the bacterial ribosomes is a 70-S ribosome and contrast that to our Eukaryotic 80-S ribosomes. So. Just a few other few other things I want to add here though...You will see the—so here we see the mitochondria, uh, er mitochondrion for one of the (mitochondria would be plural), and the chloroplast. So, the mito—eh--the plant cells have both, mitochondria and chloroplasts, and our human cells have mitochondria. Both of these organelles have their own ribosomes, and the ribosomes are—are70-S ribosomes. So uhm. The reason this important is this is where the endosymbiotic theory, or at least parts of it came from the idea that, uhm, eukaryotic more complex cells evolved from—from smaller cells actually starting to work together so, uh, the thinking is that what is the mitochondria or chloroplasts today would have been single cell organisms in the past so the fact that they have this prokaryotic, uhm, ribosomal structure inside of the them, is—is one of the uh, the tenets of that theory. The reason I want to bring this up though, is because that means that humans do have some—some 70- S ribosomes. Reason this matters, is because a lot of the antibiotics we take are—eh—they actually are attacking the 70-S ribosome to kill bacteria, but shouldn’t that mean that there’d be some impact on humans? Now h—here’s what I would say about that. Some people say “NO” because the mitochondrial membrane would keep the antibiotics out. I don’t actually agree with that, and again, this is just interesting, I’m not...not NOT saying its proven. But, uhm. I think the reason we don’t see a lot mitochondrial dysfunction when we take antibiotics is because we’re not using our mitochondria to the full capacity. I work with lots of athletes, right, I used to work with professional athletes, Olympic athletes, college athletes. And I’ve found that when—when athletes take antibiotics, they’re just trashed, right, for—for, uh, quite a bit. And I—so, I think that part of it could be changes to the microbiome, and part—part of it could be that the mitochondria are being impacted, so, you just kinda just sitting and doing your job and even spending some time on the treadmill, you’re never really...red lining your mitochondria—you’re never really forcing them to work peak capacity, so I think that’s probably why we don’t see it, but we do see it more in elite athletes. So, just kind of interesting. So, when you take antibiotics there is the potential at least for your mitochondria being impacted, and I think some antibiotics actually been shown that is the case so. But that’s why. So, your mitochondria, and the chloroplast, and the plant actually have the same 70-S ribosomes that bacteria have. So. Uh, one more really interesting thing here...is that, uhm, these are called polyribosomes; so the—one of the advantages of being a bacteria i-is that you don’t have a nucleus, and that sounds crazy because the nucleus’s job is to protect DNA, so, our DNA—DNA is definitely more protected than bacterial DNA. But, from a speed standpoint eh—think about it in our cells: transcription of DNA into RNA has to be complete; and then the RNA has to be cleaned up and processed; then the RNA has to leave the nucleus to go find a ribosome. So—so, protein synthesis is, relatively speaking, slow in—in—in humans. In bacteria, since there isn’t a nucleus, translation can begin, as you’re seeing in these images, translation can begin before transcription is even done. Uhm, RNA polymerase is actually transcribing, um, DNA into RNA, and then these ribosomes are hopping onto it and translating it into protein before its even finished. So. Just o-one of the advantages when it comes to, uh, bacteria is speed. That’s why they can produce proteins quickly. They can generate new DNA quickly. Which is why, ya know, some bacteria have generation times of twenty minutes. They’ve only been alive for twenty minutes and they’re already dividing into—into, uh, the next generation. So. So, speed is the, is one of the advantages of bacteria have. So. Alright, those are all the things I think are most interesting about the 70-S ribosomes. We’ll certainly be talking about antibiotics, and how they interfere with these ribosomes in later videos. Okay. Have a wonderful day. Be blessed.