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8. Mutants were instrumental in elaborating the model for regulation of the lac operon: a. Discuss why Piac- and lacO mutants are cis-dominant but not trans-dominan...

Question

8. Mutants were instrumental in elaborating the model for regulation of the lac operon: a. Discuss why Piac- and lacO mutants are cis-dominant but not trans-dominant:b. Explain why lacl mutants are trans-dominant to the wild-type lacl allele but lacl-mutants are recessive.C. Discuss the consequences of mutations in the repressor gene promoter (the promoter of the Lac gene) as compared with mutations in the structural gene promoter (promoter of the Lac Z gene)_

8. Mutants were instrumental in elaborating the model for regulation of the lac operon: a. Discuss why Piac- and lacO mutants are cis-dominant but not trans-dominant: b. Explain why lacl mutants are trans-dominant to the wild-type lacl allele but lacl-mutants are recessive. C. Discuss the consequences of mutations in the repressor gene promoter (the promoter of the Lac gene) as compared with mutations in the structural gene promoter (promoter of the Lac Z gene)_



Answers

Several auxotrophic point mutants in Neurospora are treated with various agents to see if reversion will take place. The following results were obtained (a plus sign indicates reversion; HA causes only $G \cdot C \rightarrow A \cdot T$ transitions).
a. For each of the five mutants, describe the nature of the original mutation event (not the reversion) at the molecular level. Be as specific as possible. b. For each of the five mutants, name a possible mutagen that could have caused the original mutation event. (Spontaneous mutation is not an acceptable answer.) c. In the reversion experiment for mutant $5,$ a particularly interesting prototrophic derivative is obtained. When this type is crossed with a standard wild-type strain, the progeny consist of 90 percent prototrophs and 10 percent auxotrophs. Give a full explanation for these results, including a precise reason for the frequencies observed.

Because the hetero carry on can produce loose scene with the presence of a mixed nucleus, one with Ellie, you plus one in l AU plus two. Um, they The mutations are from two different genes, and so in the header carry on one nucleus provides a loosening plus one, and the other nucleus provides a loosening plus two, regardless of this one losing plus one having a losing to minus and this loosen plus to having a loose seen one minus. And so they are proto tropic, meaning that the two genes complement each other. So the mutations compliment each other, and so are Gina. Types for be part are going to the led you one plus loose yet one plus in L. A. You Tu minus and Elly Yu one minus and l u two plus, and we're assuming that if these two have offspring and they independently is sort, they'll be four possibilities, so you'll have the to parental possibilities at 25% each and then you have crossing over that produces. There were confidence, so we have parent one with l au plus one in l. A. You tu minus and the second parents led view one minus and Ellie, you two plus. And then we're gonna have the to break confidence, that air possible because thes air independently a sorting. And these will also be in 25% or 1/4. And so we take the loose scene from one parents, and we're gonna combine that with the loose scene from the second parent, and that will give us one re confident. And then we'll take the loose seen from the second parents and combine that with the loose scene from the first of the other parents. You can flip flop fees, but I wanted you to see where they came from. And so you can see that in the offspring, 25% will have Ellie. You one plus in a two minus 25% will have a one minus and a two plus, and 25% will have a one plus and a two plus, and 25% will have a to minus in a one minus. And that's your Gina to the golf spring, a soothing independent assortment for the jeans

In this question. We have a mutated operator. Cold wack. Oh, see, And black OSI is going to block are no more oppressive from finding. So let's say that different shape here and or no oppressor but like this is not gonna able to bind here. I get only with documentation. So one way that we could combat this and restore no functioning is to go back up to our work hygiene and introduced a new mutation here We call this lack. I see until we know that black eye produces repressors. So if we have a mutation, we could get a kid repress er that will fit on a lack O. C the new irritation and continue to oppress prescription, yes.

So here we have three mutants of E. Coli asia having trouble producing trip open and product some producing too much of it. Some too little mutant. A apparently is constitutive. Yeah, that is. It produces uh the end science to produce trip to fan nonstop. Nothing is stopping it. It continuously transcribes the gene. Even then it's unnecessary. We also know that the mutation is inside the Oprah on. This is important because the repress your part of the apron is not considered as a part of an Oprah. It's separate from an Oprah on the Oprah. Uh Mostly consists of the promoter operator and the gene and the repressor could be distinct from the actual over on mutant B is the exact opposite. It does not produce any of the enzymes necessary for a trip to found production. But here also the mutation is somewhere inside the Oprah on. Yeah. Okay. Um, mutation C does not have a mutation in the opera. Oh, but is also constitutive, Constitutive. It also continuously produces the enzyme necessary for cipto fan. So uh how are these mutants different? And they all have mutations but at different locations in this gene drawing that I drew above. And even though mutant and mutants er both constitutive, they have mutations at different locations. So that's even more interesting. Well, let's first investigate uh where possibly mutual aid would have a mutation and we know that it's continuously uh quoting for enzymes that actually work. So the musician might not be the gene because the product quality is the same. It might either be in the Oprah on or the repressor not in the promoter. Because if there was a promoter mutation, then transcription would not happen because promoter attracts the Iranian preliminaries to start the transcription. In the first place here, we were told that the mutation is inside the Oprah on. So it's not the repressor because uh professor is technically not part of the apron. And if the operator itself is not working, that means nothing is telling the gene to stop transcription. And that's why mutant is continuously constitutive. So operator it is from U. S. A. Newton B. Is not transcribing at all. That means um and it also has a mutation inside Oprah on. If it's not transcribing at all, then most likely we don't know how the product would turn out. So the mutation is unlikely to be in the gene which is causing such behavior. If the mutation wasn't an operator that would prevent it to stop. But promoter is mainly the factor that initiates a transcription meeting B. Is not initiating transcription at all. So for this woman promoter seems like a good candidate. Mhm. Mhm. For mutants see, we were told that the mutation is not part of the Oprah on, but part of the repressor repressor gene codes for a repressor that goes into and binds into the operator. Once we have enough of the product left in a repressive Oprah on. Especially If it was induced bubble one it would induce and promote transcription. But here we are talking about a Trp Oprah on which is a repressive ble Oprah on. And if the mutation is not in the operator like mutant aid, then it most likely would be in the repressor. Because if the repress is not working, then again, there's not that uh external factor that tells the gene to stop transcription and that's why I'm eating. See continuously child crowds is gene to produce more trip to fan even when it's not necessary. I hope this helped clarify this question. And thanks for watching.

Ocean here fast. How many danger to find my eight mutations. So, essentially, if we know that two different mutations here map to a single locus, we know that the F one cross with first of all, show that meeting. So if they're not like that, would show the ball type fina type. However, based on the given data here, we conclude that there are going to be two genes on another mutations. 123456 and eight are going to belong toe one gene mutation seven here belong to the second she


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