Hi in this video we're gonna be talking about the trip opteron and attenuation. So the trip optima Ron or the tryptophan opteron pretty much is responsible for encoding genes that synthesize and process the amino acid tryptophan. And so that means that if it's the trip opteron, typically these things are regulated by themselves. So the trip opteron is regulated by tryptophan but it does. So in two different ways it's one is a repressor and this is the more like intuitive way that makes sense to us. And then the second way is through a process called attenuation and we're gonna talk about this in a second. So we're gonna first talk about the repressor because that's the one that makes the most sense. So if tryptophan is present in the cytoplasm so you have this amino acid is present, you've either eaten a lot of turkey. Tryptophan in turkey or you know you've eaten other foods or whatever. Um and in this case it's the pro carry optics cells. So it would be the pro periodic cells eating turkey essentially the pro chaotic cells have tryptophan in them either from consuming it or making themselves however they got it, they have tryptophan in the cytoplasm, it acts as a repressor and we actually call it a co repressor because it actually binds to a repressor as well. So there's two repressors here trip to fan and then another repressor protein and tryptophan regulates the trip opteron. So what happens is if tryptophan is present, it will bind to its co repressor. Its second repressor and this will bind to the operator and repress transcription. So here we have the trip repressor by itself, it's not gonna bind. But if the repressor is bound to trip to fan here this will bind to the operator and stop. There would be no transcription of this um opera on. And you can see the opera and there's a bunch of different genes here and all of them are responsible for sort of making um and processing trip to ban. So if trip japan is present in high levels, if it is present there it's gonna bind to this repressor and stop transcription. So that is the first way that the trip operation is regulated and it makes sense. Now notice this is opposite of the lac operation, right? And the lack opera with lactose is available. It binds to the repressor and that causes transcription. But here in the trip opteron the tryptophan binds to the repressor and that stops it represses transcription. So make sure you don't get those mixed up because they are actually opposite of each other. So that let's now move on to attenuation

Okay, so now let's talk about attenuation. So attenuation is actually a processes that uses T. RNA. Is attached to trip to fan to control or regulate the Oberon. Now remember tryptophan is an amino acid. So that means that it has to be able to attach to T. R. N. A. So that it can be added onto poly peptide chains when proteins, proteins are created. So attenuation takes advantage of the fact that it's an amino acid regulating its opteron because it has the ability to do that through the repressor with the presence of tryptophan itself. But it also has the present debate to be able to do this with A T. E. R. N. A. Right? Because if there's a lot of tryptophan in the cell then they there's gonna be a lot of trip to Fan TR N. A. But if there's not a lot of trip to Fan in the south then there's going to be very little Trip to Fante RNA. And so that is a second level of regulation that we're going to talk about. So first I just want to give you the summary because this gets really confusing. So I want to give you the summary of what this how the uh how tryptophan concentrations regulate tryptophan opera through attenuation and then I'll explain how it happened. So when tryptophan levels are high. Like I said there's going to be a lot of trip to Fan TR N. A. And that is going to turn off and repress the trip opera on. So let me tell you how that is. And the reason that is is because the trip operation has a little bit of a different structure than the lack opera in which we already talked about. So the Trip opera contains a sequence called the leader sequence. And this is 100 plus nucleotides, sort of. Each book has a little bit different, 100 and 4800 and 62 whatever, but it's 100 plus, but it's around 100 and 50 160 140 ish. And this is prior to the stop start side of transcription. But after the promoter. So remember we had Prague talked about Prague and so it's going to be prior to the start site. So it's gonna be before here and it's gonna be after the promoter. So somewhere in the operator region around that region, um and this leader sequence, it's a sequence of D. N. A. Right? And the sequence actually has the ability to fold in upon itself and form secondary structure by combining different combinations of four small sequences. So we call these sequences regions 123 and four. And so these form two types of structure based on how they fold. So the first structure is called a terminator structure. And what happens is that regions one and to form a loop and regions three and four form a loop. And so if this structure forms transcriptions terminated, which is why it's called a terminator. We also have an anti terminator structure where two and three form a loop instead and this allows transcription to continue. And so this is what it looks like. So we have our promoter, our operator our leader sequence and the jeans. And we have regions 123 and four here. These are D. N. A sequences. Remember we're talking about promoters all of its D. N. A. So the terminator sequence happens when one in to form a loop here and three and four form a loop and this will stop transcription. And really to be honest with you, the important structure here that stops transcription is actually the second loop here. Three and four. So even if one and two don't do this as long as three and four forming a loop that's going to stop transcription. Then we have our anti terminator. And this is formed when two and three form a loop. And this allows for transcription to occur. So now knowing that let's go back to the trip opteron. So we can use this leader sequence to control transcription and translation because it contains many tryptophan code ons. So what happens? So trip to fan levels are low. There's gonna be little tr nay. And therefore when the ribosome attaches onto the M. RNA sequence, translation stalls when translation stalls the two and three. Remember these are the D. N. A sequences and we can deal with protein and D. N. A. At the same time right? Because in pro carry out ICC cells transcription and translation can occur at the same time and that's because they're happening in the same compartment eukaryotic cells that can't happen because it's happening in the nucleus. And then translation happens in the cytoplasm. But pro periodic cells don't have that problem. So as this trip operation is being transcribed, what happens is it responds to the tryptophan levels. So tryptophan is low, there's little TR N. A. And translation stalls because it reaches those trip to fan code ons and it's like oh I don't have any T RNA I don't have any trip to fan to adhere. So I need to sit and wait until I can get some. So while it's sitting and waiting what happens is the two and three form a loop. And if you remember the two and three loop forming forms an anti termination sequence. And so this will actually promote transcription. Now this is a little bit backwards right? Because if you think if translation is stalled that means that um there won't be any gene produced. But actually what happens is the translation stalls. And that allows for transcription to take place. And when transcription takes place eventually that translation will catch up because tryptophan levels are low. They're not absent. Eventually the rivals that will find some T. RNA with TRIPP van on it and continue that process. Um But because they're low that causes that stalling while it's looking for it and that allows the anti terminator sequence to form and transcription to occur. So it's a little bit counterintuitive than what you would think. So when translation stalls because it's low transcription increases that means that the opposite happens. So when tryptophan levels are high then that means there's a ton of trips of anti RNA and translation doesn't stall, it just continues and because it continues it actually reaches a stop code on at the end of region. Once I remember we had the leader sequence 34. So there's actually a stop code on right here. And if translation doesn't stall and it just keeps going it reaches that stock code on. And when it reaches that stop code on. What happens is a loop between three and four form and that acts as the terminator sequence and transcription stops. So translation can keep going that will form that terminator loop and transcription stop. So let me show you what this what happens here back up. So if we have low trip to fan what happens is the river zone. So things are trying to transcribe. And the low trip to fan causes the ribosome to attach and it has no it doesn't have a lot of T. R. In trip so it stalls, right the ribosomes stalls and it sits here for a little while while it searches for that T. R. N. A while it sits there, what happens is the two and three will form a loop And when that happens that allows transcription to continue because this is the anti terminator structure and transcription can occur if that structure forms on the other hand, if you have high trip to fan, what happens is that this just goes quick, right? It doesn't need to until it encounters a stock coat on and so it stops here, creates this sort of short peptide sequence. But when it does that the three and the four um form a loop. And this is the terminator. Like I said this is the important terminator structure and this stops transcription now. If you remember back let's just go straight back up here at the very beginning. Like I said when trip to fan levels are high attenuation turns the trip to fan operation off. So that's exactly what you're seeing here. When you have high levels of trip to fan transcription is stopping. And that is because um because the apron encodes for genes that make tryptophan. But if the cell already has a lot of trip to fan it doesn't need to make more. So this level of or this type of regulation allows for the cell to say oh I have a ton of tryptophan, I don't need to make more. But this is called a tenuous because it uses these T. R. N. A. S. To affect translation and transcription at the same time. And that obviously is a little bit hard to wrap your mind around. But it does make sense if you can can look and examine and really um look into this image here. So with that let's now turn the page.

Okay. So now let's talk about the trap regulation of the trip opteron. So um pro periodic sales have been around for a really long time. Right? They just are always around, they've been around for so long and that means that they've had a long time to evolve different ways to do the same thing. And so occasionally, although we've talked about the main ways the trip opteron is regulated through their oppressor and the attenuation. But occasionally a few organisms have evolved an additional or separate way of regulating the same opera on. So the one that I want to talk to you about was done by this organism here and it uses a special protein called the trip RNA binding attenuation protein. So what happens is that this protein binds to trip the van. And that means when tryptophan is high. This trap protein is bound to a lot of trips to fans meaning we call that saturated, right? It's bound to a ton of them. And this trap protein will then bind to the leader sequence that we talked about before when it binds the leader sequence that forms the terminator configuration and stops transcription. Now what happens with tryptophan is low? So when tryptophan is low, another protein comes in called the anti trap. And that binds the trap instead. And so when anti trap binds the trap, this allows for the formation of the anti terminator configuration and that promotes transcription. So the trap anti trap regulatory method can actually be sensitive to a wide variety of tryptophan concentrations because you're looking at you're dealing with saturation or trap buying some multiple trips to fans. So there can be intermediate phenotype for when trap is bound everywhere it can be saturated versus when it's bound to half of the tryptophan molecules. Um So that binding isn't as strong. So what this looks like if you have high levels of tryptophan you have trapped this gray approaching here, binding with tryptophan these red dots and this forms the or the terminator sequence and that stops transcription. And then when tryptophan concentration is low you have trapped and anti trap bound. This forms the anti terminator and that allows for transcription to continue. So this is just one of many ways actually that pro periodic cells have independently evolved how to regulate the trip to an opera. Now the repressor and the attenuation is definitely the top two main ways that pro cryonics do this. But I wanted to mention this because first it's mentioned in your book and you may need to know it but second because it really highlights the way that pro carry optic cells don't necessarily all regulate the same gene the same way. And so um many of them because they've been around for so long have evolved sort of independent but similar ways to regulate the same opera. So I've been telling you about the main ways and those are the most important. Right? Those are the big examples to know but know that there are so many different ways to regulate the same thing in pro periodic cells. So with that let's not move on.