Hi in this video we're gonna be talking about spontaneous mutations. So the majority of DNA mutations that occur in organisms are spontaneous And the reason that I can say this is fast and I know this is true is because of an experiment done by um two scientists. I'm gonna butcher their names but Lauria and Del bronc and they did this test called the fluctuation test. And they are the ones that proved that the majority of the organism mutations are just spontaneous. So what they did is they had to bacterial cultures and they tested for their ability to develop resistance to a virus or bacteria page. So they grew to different bacterial cultures and expose them to different conditions. And asked about resistance to license remember bacteria pages they enter the effect cause license bursting of that bacteria. So they used these bacterial cultures to look for license of bacteria and when they didn't like that would be an example of resistance. They were resisting that infection, resisting that license. So how the experiment was designed was they had two cultures. One had 20 individual small cultures and this was grown in the presence of the page. So the bacteria fage was put into these cultures and those bacteria were grown while they were exposed to the virus. The second one was you had one large culture and this was not grown. So this was page was not there. So this had page. This did not have page and they wanted to look for resistance. Now their hypothesis was that if it's spontaneous then it's not going to matter whether or not the bacteria was grow in the presence of the page or not because the page would have the presence of the fate would have nothing to do on whether or not a bacteria developed resistance right? It would just be a spontaneous mutation. One mutation would help and one wouldn't and it would not matter whether or not they were grown Now how they tested this is after the growth they took a little bit of each culture and placed it again onto a plate and exposed it again to bacteria fage and looked for license. And so what they found is that resistance. So the development so the ability to resist that infection resist the licensing was not dependent on previous exposure to the page. And this meant that it didn't matter whether or not the bacteria had previously been exposed. The page had did not induce that mutation. Those mutations just spontaneously occurred. And so their data they found that the small cultures that had that had the page or the check mark had a range of 1 to 107 resistant colonies were the one that did not have the page had 14 to 26 And it had nothing to do. Some of the plates had won. Some had 106. And these different numbers had nothing to do with the presence of the page. So what this looks like is this column here is induced. So this would be if the page had some kind of effect on mutation and this would be spontaneous. And what you would see is that over time. So if you have a bunch of different bacterial plates that if it were indeed induced then the fade would induce the same number of colonies to resist it each time. So each one of these cases there's still two red colonies and these are the resistant colonies, right? And it doesn't matter what happens as long as the pages their age would induce it. And it would do sit in the same number of bacteria every time and therefore you would get the same number of colonies every time. Whereas if it was spontaneous you just sort of had to wait. Right? Sometimes it would be one, sometimes it would be four, sometimes it would be none. Sometimes it would be too. And this is what they saw. They saw that the spontaneous um had different number of colonies and that it was just a spontaneous that had nothing to do with the individual. Um The induction from the page. So knowing that organisms undergoes most of the time undergo spontaneous mutation and that's what causes mutant organisms. What are the different mechanisms that lead to this spontaneous mutation? What causes these spontaneous mutations? Well, one potential is errors in DNA replication. Right? We know that D. N. A polymerase has um is it perfect? It does make mistakes. Um and typically d errors in DNA replication due to the Plymouth race cause things like transition trans versions frame shift in del etcetera. All those different types of mutants that we talked about previously. There can be naturally occurring DNA damage and this is DNA damage that um you know, can sort of just come from the sun. The UV light causes damage and that's just sort of this natural thing that happens. Um And this causes different types that we haven't talked about yet, but we'll talk about things like deep urination, delamination. These are all different terms for just like changes in the basis and well, we don't we don't need to know them right this second, but we will talk about them in future videos. And then a different, another way that this could happen is through automatic shifts. Now, some of you some of your chemistry people might be more familiar with Todd Sommers, but essentially what they are is different forms of the basis. So A. T. C. And G. Which differ bases on the position of protons and there's many different forms. So that means that every base A. T. C. And G. Comes in multiple different taught summer forms based on positions of the protons. Now so far in genetics. And I'm sure in biology you may be a little bit surprised about this because we only talk about the most common ones, right? A. T. C. And G. Those are the four most commons and they do the most common pairs right? A. Pairs with T. C. Pairs with G. But top tumors can have slightly different pairings and they can form pairings that R. A. N. G. And T. And C. And they do that naturally and that can cause some mutations these spontaneous mutations. So an example of this is this is Euro sell. These are two different forms of Euro sell but they're different top tumors meaning that the protons are sort of different in these two. But it's still your cell and these different Euro cells have different binding affinities for different bases. So this you each one of these you may or may not bind to T. Like it should. Now finally I want to talk about diseases that can arise in humans from spontaneous mutations and that is a major one of these are trinucleotide repeat diseases. And so these diseases are exactly arise exactly how they sound like they are due to the addition of nucleotide repeats, specifically tri nucleotide repeats, which means three. And so you add these extra code ons essentially onto this gene. And so the generally everyone has these repeats. Right? There's usually some gene and it contains a number of repeats. But disease individuals usually have more. So an example of this is that's using your book as fragile X syndrome. And normally normal people being you without fragile like syndrome contains 6 to 54 repeats of C. G. G. In this one gene. But people with fragile X. Syndrome contain many more that contain 200 to 1300 cG repeats. And um obviously this is due to addition of more CG repeat. So how is that added? These are spontaneous editions. And what's the mechanism of adding those nucleotides? The mechanism of adding those nucleotides called strand slippage. Which is how this fits into the whole mechanism section. And so strand slippage and cause causes insertion of D. N. A. And can cause insertion of these nucleotides. And so what happens is that these nucleotides are there's a lot of them and they're repeating. And so those are a lot of sequences that are similar. And when those sequences that are similar are being um transcribed or replicated, that creates D. N. A. That can easily bind to itself. And when it binds to itself it forms a loop. When it binds. When it forms that loop it loops out a bunch of different repeats. Right? You could have probably 30 repeats right here. And even though the polymerase for instance in replication has already read those and it's already copied them if they loop out, that means the polymerase goes back and does it again and can add those nucleotides twice because now the strand has like bunched up and it doesn't realize that it's already read right because it's just binding and reading. And if this strand is bunched up it kind of gets stuck and it just keeps reading those um those same nucleotides over and over and over again. And so strand slippage can really cause these large insertions of D. N. A. And may at least in part if not in full, which we're not sure if it's simple or not. But in part cause these trinucleotide repeat diseases where normal individuals have this small number of repeats but disease individuals have a lot higher number of repeats. So these are spontaneous mutations and just a few mechanisms, not all of them but a few of how spontaneous mutations occur. So with that let's now move on.
Which of the following tests determined that most mutations are spontaneous?
Luria and Delbrünk fluctuation test
True or False:Thymine tautomers can base pair with cytosine.
Which of the following forms of DNA damage is NOT caused spontaneously?