A fellow student considers the issues in Problem 22 and argues th...

Question

A fellow student considers the issues in Problem 22 and argues that there is a more straightforward, nongenetic experiment that could differentiate between the two types of mutations. The experiment requires no fancy genetics and would allow you to easily assay the products of the other SOS genes. Propose such an experiment.

Accepted Answer

Hi everyone. Welcome back. Look at our next problem. It says the blank is a universal reaction to DNA damage in which DNA repair and neurogenesis are stimulated while the cell cycle is halted. So let's notice when we look over our answer choices that three of our choice is a basic decision repair. See mismatch repair and D. Nucleotide excision repair have the word repair in them. Those are all forms of DNA repair. But when we look carefully at our question, it asks for the name of reaction to DNA damage in which DNA repair is stimulated. So we're not talking about the repair itself, we're talking about a reaction that causes repair to take place. So even if we didn't remember what it was that would help direct us to the correct answer which is choice be the S. O. S. Response. So this is a response that's one of the things that initiates DNA repair. Um We know we have various repair mechanisms that take place during DNA replication that sense errors in the newly synthesized DNA strand. The S. O. S. Response is as indicated by its name um an emergency response to severe emergency response to severe D. N. A damage, severe and extensive DNA damage. So to the point that the cell replication is going to completely stop and in fact a cell might even go on to apoptosis because there's so much damage. Um a common cause of this would be UV damage to a cell which can be very extensive. So that's when our S. O. S. Response gets called in. So let's just recall briefly that process. I will put up a little diagram here we recall that the S. O. S. Response is regulated by the S. O. S. Opera on. This is an induce a ble operation. So it's a default state is off obviously when nothing's wrong in the cell. Um And it will turn on. It has a repressor, the lexa repressor that sits on the operator most of the time and then it has an inducer. This wreck a protein. And the wreck a protein is activated by the presence of single stranded DNA. So we've got this damage D. N. A. The wreck a protein is activated as a result the wreck a protein then cleaves that lacks a repressor protein causing it to fall off the S. O. S. Operator. This then allows RNA polymerase to bind to the promoter and expression of S. O. S. Genes to go through. However it's not quite that simple because there's different S. O. S. Genes controlled by that opera on and they respond according to how much damage. So the first gene is transcribed to see if that will do the trick and if it doesn't then it goes on to even more. So let's just remind ourselves real quickly of those different genes. So now that we have our S. O. S. Opera on um is no longer repressed. That's been turned on. This emergency response takes two stages. The first gene expressed is the N. Er enzyme nucleotide excision repair um which can cleave out damaged portions of D. N. A. And repair them. Um However if there's too much damage for this to repair those lexei levels drop further because since you still have damaged DNA you're still going to have activated wreck a more lexei um gets cleaved and you have more, the S. O. S. Opera continues to be expressed. Then you go into expression of D. N. A. Polymerase five um for trans lesion DNA synthesis. So if you think translation across lesions, this synthesizes DNA by actually bypassing lesions in the D. N. A. As you can imagine, this is very error prone because if you're just skipping these damaged areas you have a lot of errors introduced. So this is kind of the last ditch effort to prevent cell death because again you're talking about damage so severe that the cells are destined for apoptosis without some sort of intervention. So that last stage of the S. O. S. Repair is this last attempt to prevent cell death but as a result is very error prone. So that's um the S. O. S. Response as we recall. So let's just briefly look at our answer choices again, we've talked about how they're all repair mechanisms. Uh not this reaction that generates them but we'll briefly take a look at them. So Choice A. Is basic cision repair. Um This is one of these repair steps that goes along looking at the newly synthesized DNA strand. It happens throughout the cell cycle. So we know our S. O. S. Response happens when the cell cycle is halted. Basic cision repair is part of that process happening as we have newly synthesized DNA. And it repairs helix distorting lesions in that new strand. So it's not our answer because it's not what happens when the cell cycle is halted. Again, it's a method of repair. Not this whole response that generates repair. Oh I see mismatch repair is similar. Um It's part of the repair process of the newly synthesized DNA strand comes along um to catch any mistake or base pair mismatches that the proofreading enzymes have missed. So again that deals with base mismatches as you can tell by its name. But again happens throughout the cell cycle, not while the cell cycle is halted. And finally nucleotide excision repair um deals with larger areas of DNA damage. And it's part of the S. O. S. Response, but it's not the response itself, which is why it's not our correct answer. So again, the B. S. O. S. Response is a universal reaction to DNA damage in which DNA repair on neurogenesis are stimulated while the cell cycle is halted. See you in the next video

Key Concepts

Types of Mutations

SOS Response in Bacteria

Experimental Design in Genetics

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