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BIOL 2321_16323_Microbiology for Science Majors - 04_11_22_Lecture
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00:02 Okay. Folk groups me and Michael's here. Okay there we go.
00:09 Welcome. So we've got uh let's . Week 13. So we got
00:16 two more weeks and then a may I think is um we ended here
00:23 anyway coming down to the wire. uh today we'll finish up unit three
00:27 we don't have that much to do . So just a little to finish
00:31 check 10. So um reminders I sent an email this morning.
00:37 the exam at the end of the uh you know you have questions about
00:41 , email schedule of teams meeting, have you? Fine. Um So
00:49 quiz. So we're gonna start unit uh let's start unit four on
00:56 And so that will take us to so remember there's there's no comprehensive final
01:03 . It's just jam four is the and that's just The material will will
01:08 covering on Wednesday. Okay. Um see. Smart work. Uh the
01:15 10 is not due until tomorrow. nothing nothing else this week. That's
01:21 . Unit for stuff. Not due another couple of weeks yet. Um
01:27 so I'm gonna finish chapter 10 So um let's see. So uh
01:34 we went through so really today is just looking at some examples of because
01:40 been hammering on um really these examples trans transcription of control bacteria. So
01:47 transcription of control. It's really so can allow the army plum raise to
01:54 to transcribe or not at all. so it's not even about controlling the
02:01 that transcripts. It's before that Right? So um and so we
02:05 the black lactose opera on um trip opteron uh both of these involving the
02:13 or activating a repressor in different Um But the end result being um
02:21 were either allowing or not allowing transcription occur. Right? And that's that's
02:25 definition of transcription control. Very common mechanism in precarious gene control. This
02:32 transcription of control. So but then looked at uh in this additional um
02:41 in a trip to fan control, attenuation mechanism. So whereas this part
02:48 here right, the active activator activator . This controls that's the bulk of
02:56 control in this mechanism. But the bit of it that uh it's left
03:00 to do is done by the continuation . Okay. And that again,
03:05 though you see arriba zone being involved this, Okay, it's still is
03:09 transcription of control. It's just that of the ribosomes position is determining whether
03:17 not transmission occurs. Right? So went through, you know how that
03:21 and it's position a it's based on leader sequences that occurred prior to the
03:31 structural genes showing purple here at the of it. Um And so and
03:37 formation of these stem loops that occur the RNA. So does occur here
03:43 or 23 and so on. And gets about the proximity of that loop
03:50 to these memories, shorter distance longer distance there. Um Really the
03:59 of the loop in the low tryptophan scenario has really no consequence because it
04:03 do anything. Okay. But it spontaneously. Okay. And it forms
04:09 the positioning of the tribal zone covering or not covering up the two reasons
04:14 , whereas appear uh derived from its that two regions. So 3434 preferentially
04:22 . Okay, and that's closer to to the preliminaries and then that physical
04:27 knocks it off. And so before it gets into the structural genes
04:31 . Okay, and again, How all relates 1, 1 then falls
04:36 next and falls to next. It's of the positioning is all based on
04:41 it stalls or stops. Okay, installed the trip code ons for at
04:47 natural stopping point. The stop code and that determines which loop forms.
04:54 then that relates to. Okay, does it stalled at the trip?
04:59 the quality of the phantom, so a charged TR N.
05:02 Or uncharged in this case. To make that a charged tR
05:06 A. You gotta have a trip fan added here, right? That
05:10 has to be connected. Okay. it relates absolutely relates to what's the
05:15 of trip to phantom. This Okay, so this is kind of
05:19 what it's all about. Is this . Okay, but then, are
05:23 forming charged or uncharged? That is by the quantities of defending itself.
05:29 that then we'll go to the And so yeah. Hi are
05:34 Fan stalls here are stopped there. Whether where it stops which loop forms
05:43 doesn't knock off the deliberate or So it kind of all related.
05:47 . Um there was there was there questions about that your mechanism?
05:52 Yeah. Work well in many attenuation . Yeah. Okay. So attenuation
06:02 occurs. So like I said, know I don't know the exact percentage
06:08 I was Make a rough guess and that let's say that 99% of the
06:14 occurs through this mechanism here. Active actively press it. Right? So
06:19 that the binding here um It is irreversible. Obviously can come off and
06:25 . Right. And so let's say in a scenario where it's inactivated or
06:30 activated repressor. Right? So it's to the operator. Right. Even
06:34 that scenario it comes off a small of the time but it can come
06:40 because it's not an irreversible binding. . And so those instance, so
06:44 is kind of one of the ways clamp down on it. Okay,
06:47 we do get a little bit of . Right? So obviously we don't
06:51 that to happen. Right? Because in in this repressed mode. So
06:56 when that little bit of that that occur, you have this as a
07:00 because the leader sequence will be transcribed . And then you get the whole
07:04 thing occurring. So it's kind of that's the logic behind this. Does
07:08 make sense? Okay. Um and questions. Yeah. And we saw
07:14 same thing in the lactose opera you we say yeah it's it's it's um
07:21 is shut off. Okay but we get a little bit of expression and
07:26 a good thing for the lack of because you have to make that black
07:29 the the lactose detector I call it instead approaching that sits in the membrane
07:34 brings lactose in. But it's the the soul can see lactose. And
07:38 you have to make a little bit that even in a scenario where it's
07:42 repressed. Okay. But it's the way you can just sell can never
07:46 lactose is to have have a couple molecules worth of that sitting in the
07:50 . Okay. So it all goes to you know the in any
07:55 You know, molecules binding to each . Right. Protein protein um protein
08:01 . N. A. Right? things are are rarely but they're usually
08:07 irreversible. There is some level that still you know off fine. Just
08:12 conditions will determine typically how much it's and not now that's what we called
08:18 constants. And so these numbers can depending on conditions. No questions.
08:25 . So so we're gonna get away now Just well just look at some
08:32 of control beyond the transcription control. the first one we'll look at is
08:38 example of transcription control. That's a response. But the other three are
08:43 of a little bit of variations from . Okay so the stringent response.
08:49 so there there are a number of that get uh expressed when cells are
08:59 different kinds of stress. Okay. one of those could be if it's
09:04 endospore forming bacteria in the hole nation may kick in if if it's capable
09:10 doing that um other stresses like ph , um uh radiation you know stress
09:20 uh these are things when certain or as we'll talk about in a
09:25 Um or starvation. These are all that are gonna stress the cell
09:30 And so in that kind of condition going to go into survival mode.
09:36 try to turned on express different genes will enable it at least. The
09:43 is to prolong how long it can viable. Of course. That varies
09:48 microbe to microbe, the capabilities and conditions. And so this is a
09:52 of a very uh common um The stringent response is all about the
10:00 response. Okay so stringent I guess textbook definition it relates to stringent limit
10:06 limiting. Right? Stringent actually means I'd say. And so when um
10:13 resources are diminished. Okay again that's a stress condition. So he wants
10:18 survive. So what do you Well you you do things that minimize
10:25 output And uh so you're you're not do functions that you don't need to
10:30 doing in that kind of condition. . And one of those is to
10:35 vibes um formations. Remember to make zone right? You have to transcribe
10:42 RNA molecules, lots of different proteins rivals are collections of RNA molecules and
10:49 of proteins. Okay so you have do so in any healthy functioning cell
10:54 synthesis is probably the most abundant Okay to enable that. You've got
11:01 make lots survives homes that that will that out for you. So it's
11:05 it's a big activity in the You know you we've all seen the
11:08 pictures of a pro you carry out right all the dots that are in
11:13 right there. All ribosomes. So in any cell protein synthesis is
11:17 to be a prime function. So requires lots of ribosomes. And so
11:21 of the first things to do if in a stress condition is to let
11:26 production of these things. Okay, what the stringent response essentially is.
11:31 . And so procreate ribosomes have this activity associated with it indicated by the
11:40 . E. L. A. L. A. Okay that's associated
11:45 the tribal zone. And so in when um so how would arrive at
11:51 ? Since when something's not going It kind of relates to think of
11:54 attenuation mechanism right? When when it low on trip to fan and it
11:59 to those adjacent trip cardin's installed. ? So um starvation will will begin
12:05 produce transfer RNA molecules that aren't Okay. And so when these coders
12:10 to pop up the ribosomes translating, was not a charged T.
12:15 To go there for the amino So it stalls basically can go
12:19 And that's that's really the indication that response probably needs to kick in and
12:25 stalling activity or idling. They call often idling ribosomes right there moving in
12:31 not going anywhere. So that triggers activity. Okay PVC here and it
12:39 this signaling molecule called uh guana seen phosphate, right? For phosphate.
12:49 and so that uh interacts with Preliminaries and so specific specifically to reduce
12:56 expression of of lots of different genes especially those that are are are in
13:03 jeans bibles. Omo RNA. Okay are needed to produce ribosomes. Okay
13:10 again all in the effort to part the collective effort because not just with
13:14 general response this particular response occurred but things stress responses occur as well to
13:19 of again to to minimize energy output needlessly as well as to you know
13:27 it in the mode where we can . So can I. But this
13:32 responses is really among prepared. Universal of response. Um But it is
13:39 transcription of control because it r it interfering with memories right? So you
13:43 if you're on and either allowing or allowing in this case to transcribe.
13:48 a transcription control mechanism. Um Many about that. Yeah. Oh it's
14:00 reaction. So that Rail A is associated activity with the rival zone.
14:06 that catalyze is um uh takes a lies a teepee and then adds a
14:12 to the iguanas in tetra phosphate So G. T. P.
14:16 . Three hybridized a teepee. And floss for lead GTP and that gives
14:21 four. Now you have Guantanamo tetra . So it cries interview to do
14:26 . Mr Rogers. Yes. Well Rail A is an enzyme associated with
14:31 ribosomes that does that activity. So it stalls it kind of our items
14:36 do do do nutrient limitation. Then kicks in the activity that then produces
14:41 guangxi tractor phosphate. Yeah it comes . Yeah that's that's pretty much
14:48 Yeah. Yeah. It uses energy go into starvation mode for that effect
14:58 that little bit of energy will create cell wide effect. So you just
15:03 to do a little bit because that's a it's probably a mechanism to kind
15:08 ensure like you said if it's going produce energy. Well it must be
15:12 it for a reason. Right? because that little bit of energy produced
15:17 that doesn't have to produce a lot I'm going to see a type of
15:21 to get the effect. But it have to do that phosphor relation.
15:26 a I don't know I was I looking at it and I give this
15:35 thursday I should have looked it up I was at that time was going
15:39 does the ariel actually stand for? I wish I could tell you but
15:42 don't think it's a protein. Right terrible. Um I guess I
15:54 think they call it either but you you could stretch it and go since
15:59 it's activating is producing this G. . P. D. Etcetera phosphate
16:05 . And that actually is the one affecting the expression. So I wouldn't
16:10 it an activity because it's not acting a promoter or anything but it eventually
16:14 trigger a molecule that is has some that that has some of that
16:20 And so it inserts itself once you energy sources and, yeah. Right
16:27 that respond particularly the idling ribosomes. must be someone in binding between the
16:31 and then the is not just kind move move somewhat moves in place on
16:37 . That confirmation change slightly. Might what affects the L. A.
16:42 the distance because really is kind of with it to a degree. And
16:47 maybe it senses kind of when the zone positioning is changing in that then
16:53 kind of activates it. I'm not they actually know what it causes
16:57 So it's an activator to deactivate. I would just say get activated in
17:02 head. It's a it's a signaling . Well it's a molecule that forms
17:09 another molecule that they can affect expression you want to call it a pre
17:17 . I thought that yeah. Yeah. Right. Right.
17:22 Right. Um A lot of times are kind of involved steps multiple steps
17:30 can kind of modulate the response. rather than being just a offer on
17:37 you can kind of modulate the response typical in biological systems. It's it's
17:42 it's all or nothing but sometimes you a number of steps there to kind
17:46 fine tune or kind of modulate the effect. That makes sense any
17:54 Okay so the next example So this one that's so you went to the
18:04 the levels of control. Right so have get transcription control you can have
18:09 control, post translational control, post of control. Um Those you know
18:18 could there is no kind of term that for this one. This is
18:23 control at the level of D. . A. Is the best way
18:26 describe it. Okay so a couple ways that can be done. One
18:32 to modify nucleotides that can that can expression. Um this is another
18:39 This is common in a number of pathogens. Okay. Uh and we'll
18:47 it again in the next unit when talk about microbial pathogenesis. So um
18:56 a pathogen um it also relates to your adaptive immune system. So your
19:03 immune system which we'll talk about next um is uh system of specialist cells
19:12 that. Um So in a nutshell data, immune system depends on recognition
19:21 a pathogen and then the recognition leads a binding and that binding leads to
19:27 response in the most basic terms. that's what it is. Okay.
19:33 And so um the recognition of your system selves to it is through,
19:43 know, picture that your immune system had eyeballs. Right? You're looking
19:45 see what's what's in your body that be there. Okay, so what's
19:50 gonna see? It's gonna see the on the periphery. Right. What's
19:53 the if it's a virus, glycoprotein sticking out, Right. I Lamanna
20:00 , perhaps a capsule enclosing a you know, things on the
20:05 Right, proteins. Any kind of particular proteins sticking out these kind of
20:12 . So that's what your immune system these types look for. Okay.
20:17 so there's recognition and there's binding to . Okay and so of course the
20:23 do we call the the thing sticking of the things on the periphery of
20:28 pathogen. We call those. What with a not everybody but antigens.
20:36 ? So those are the engines that on the on the surface that your
20:40 recognizes or that your immune system cells recognize. I think about it as
20:44 learn next week there are energies associated the pathogen but there's also energy associated
20:51 you, what we call self Okay. Uh we'll talk about that
20:56 week. But um so the engines the pathogens are what are recognized.
21:01 so potentially. Okay, that recognition so that whole system of your that
21:08 immune response is not instantaneous. It's a time component to it to see
21:14 , recognize it by intuit producing That takes time. Okay. Uh
21:19 immune system like you know the physical of your skin. Right, mucous
21:25 or these are physical barriers that are there there all the time.
21:29 Ready to stop stuff. Okay. adaptive immune system because more of a
21:34 to put in response, recognize, detect, do something. Okay,
21:39 takes time anyway. So um so that but that time response, you
21:46 , that's that's something that the pathogen advantage of or can. Okay,
21:52 when um when the uh so independent your body, can you miss
22:00 recognize it response e antibodies. Um then that's that's what you want
22:07 body to do. Obviously. Now have the ability to some do of
22:14 that antigen profile. Right? So engine is basically you don't say proteins
22:20 nature can be collectible proteins in some maybe carbohydrate protein combinations. Uh glycol
22:28 in some cases but mostly they're protein nature. And of course you can
22:33 an engine by changing the the amino sequence of the proteins that comprise that
22:40 in. Okay. And if that then that can make that pathogen temporarily
22:47 to the immune system. Right? the immune system will lock on to
22:53 certain it will recognize the engine and lock onto it and increase the
22:57 But it changes then that's not then time the patrons buying time now before
23:04 gets recognized and that's when it can and multiply across disease. So that's
23:08 immune avoidance is all about. It's the energy in the past when changing
23:12 engine form, pattern type. And making it for that period of
23:19 invisible to the immune system, your system. Okay. And so like
23:23 said, it's things on the periphery LPS layer of gram negative right after
23:27 O A. Like protein spikes. I said before the virus, these
23:32 all things that are perfect. And these are things that can
23:36 Okay. Um so the example here salmonella enteric foodborne pathogen. Um and
23:47 , this is a really basic Uh It has two forms of
23:51 so is made of these little units put together called the gel in.
23:56 . And they can vary in their assets equals. Okay, so in
24:01 example we see uh so the, the genes involved after L.
24:08 B. And see right each one for a different Magellan type.
24:15 One H. Two. So in car, you see here the
24:19 two Is the one being formed. , so with the the pendulum of
24:25 salmonella and You know, subsequent generations shown are going to have an H2
24:33 for a gel and comprised of To put gel in. Okay.
24:38 so it's uh the gene itself has like an opera and and has has
24:44 promoter, right promoter. Then we the actual gene that synthesizes that The
24:51 coach for the Dillon H. two also a repressor, right? That
24:56 see here. Okay, so both those are expressed at the same
25:01 And so the repressor acts on the type. This is the H.
25:07 over here, H. One And so it's not produced because being
25:11 off by the repressor of the of H. As part of the
25:14 Two operation. Okay, so this Simon was going to produce flagellum
25:20 only the H. Two type. , now the other part to note
25:25 what's going on over here. so that's um so within that,
25:34 , here's the promoter Within that green at the very end is the promoter
25:41 the to the H. two. part of the opera. Okay.
25:47 the green part is the part that spontaneously re combine. Okay, so
25:55 H. I. N. Is so culturally recombination. It's that kind
25:59 serves to cut and paste and Okay. So what happens is we
26:04 rearranging cuts out and convert. Right orientations. Okay. Now that's all
26:13 and dandy. But the thing is when that happens. And and the
26:17 at which that happens is something like and 100 21 in I think 100,000
26:28 hmm. That's kind of the rate which this spontaneously occurs. Okay.
26:34 uh like I said, that's But the thing is when that
26:38 remember that this promoter with this segment is part of that. So when
26:47 thing that combines that promoters going with , right? And gets flip flopped
26:52 . So as you see here, recombination event here is our promoter.
27:00 supposed to be right there. that one's been flipped around because here
27:07 our gene. Okay, The two. This is the H.
27:13 . And we pressure together. And so um because the promoter has
27:23 taken away basically because the recombination Now not expressed. But the H one
27:32 okay, so that repression. The is not there anymore. So now
27:36 free to transcribe and be expressed. when that we called gina inversion,
27:43 occurs. Um that become become the flips. Okay. It takes a
27:53 with it and now it can't be in store H. Two is expressed
27:56 H. One. Excuse me So now subsequent generations the flagellum that
28:02 cell has will be the H. form. Okay, so it's switched
28:07 engine form. Okay. Um so is another kind of Picture of
28:15 Okay, once more to kind of up a little bit. So we
28:18 our h. two. Okay, . Mhm. Okay, There we
28:29 , promoter H. two. Okay repress her Walking off expression of
28:36 one which is over here. Okay then that's the scenario we have going
28:42 H. Two expressed H. No then we go, okay you
28:47 so you see how follow the promoter here it is there and then there
28:54 is there. Okay and so there's promoter in front of the in front
28:58 these genes, so I'm not gonna transcribed. Okay. and so um
29:03 . one is check um so let's at an example here of strategy.
29:13 so if you're salmonella and you're infecting person. So as you see it
29:20 , right, I just kind of them in to show you the two
29:24 types. Okay so we have a , so let's say this guy eats
29:31 that's contaminated with sound and the salmonella on that piece of food eaten um
29:40 this population has has salmonella with both . One and H. Two in
29:45 equal proportions. So from the viewpoint salmonella, is this probably the best
29:53 or would it be better? Alright let me go ahead and uh oops
29:57 about that, let me just make poll question real quick. Okay I'll
30:05 it. So you gotta you gotta contaminated food. Okay, It's got
30:12 5050 seminal, it has it's all interrogator, half of H.
30:17 half of H. One, but um just the whole shebang, it's
30:21 in your gut. Okay, so put your arm a salmonella hat
30:26 okay from their perspective, is this the best long term strategy for its
30:33 to be to have that happen this ? Um The answer on your
30:38 you have a question, yeah, the question protein recognized? I can't
30:48 only going to give you this Mhm. Yeah. Mhm, mm
31:16 . Uh huh. It's just just hypothetical question, don't overthink it.
31:30 . So you've got a population of one, right, I'm just saying
31:34 and they just happen to have 5050 each type? Right, so it
31:40 into goes into the body and so from salmonella viewpoint, is this gonna
31:44 a good long term survival strategy or , compared to what it might what
31:49 otherwise be? Right, so that's two things, you have to wait
31:52 your head. Mhm let's let's see we got. Okay, so who
32:03 um B what do you what did say? B Thank you?
32:21 two and a student. Right. . It's like you're playing poker and
32:28 know, here's what I got Call your calls out at the
32:31 All right. Everybody knows what they've you've got. Right. So,
32:35 body in this scenario, the body uh someone uh someone has shown all
32:43 cards to the body immune system Right? So it's it's both forms
32:48 be um will be recognized. Like said, it doesn't matter if it
32:53 or not. Right? So, that's not a good long term strategy
32:58 it will get found out and you better to come in with this kind
33:04 mhm ability to do this phase Better to be mostly of one type
33:10 the other. Okay. Because then the one type gets found out or
33:16 recognized, then that buys time it spontaneously. Then then the next generation
33:21 the other the other energy reform. that will, you know, again
33:26 time because it takes time for the to recognize, detect, recognize,
33:31 . And during that time knowing how bacteria grow. You know, you
33:35 have of course uh advanced disease or grow faster Hughes disease state. But
33:43 other thing is uh this is this a relatively simple example of to angio
33:47 . There's there's bacterial types that can multiple 67 between 67 different types of
33:54 for their particular type of uh Whether the capsule of what happened.
34:00 . Any questions about that? So the general, mm hmm mm
34:08 , mm hmm mm hmm mm Yeah. Right. Exactly. Or
34:14 in with H2 or whatever but have one or the other. You
34:17 make it make it like maybe 70% the population should be just one type
34:23 some something much more than half 50 . Right. Yeah, that's that's
34:29 it. Um so and with nice because of meningitis which you all get
34:37 for. That's that's one that has ability to do this and has multiple
34:42 six or seven different variations. I it's uh capsule er energy. And
34:46 believe it is. So um so successful strategy and on behalf of the
34:53 . And I think the malaria organism the same way. Um any other
35:02 ? Mm hmm. Okay. So next example, so this is
35:09 so we talked about regulars before and regulations are collections operations that are kind
35:15 have a a overall common function in type of metabolism. And we saw
35:22 those can be controlled by a common factor. So sigma factors are a
35:27 thing to control because they interact with have to commemorate go to a
35:32 Right? So of course that would a natural control point. And so
35:36 is looking at um uh temperature So again, a stress response that
35:43 saw with stringent this here we're looking the a temperature. Okay so temperature
35:48 kind of a radio. So this a heat shock genes. Alright,
35:53 heat of course it's going to be because it can cause proteins to denature
36:00 structure unfolds. News function certainly to acids can denature as well. So
36:08 heat stress. Well heat stress you to you know as best you can
36:14 keep these proteins functioning under these conditions and you do that through the action
36:20 producing other proteins that serve to kind bind to them and and maintain their
36:27 . Okay we call chaperone proteins um it all begins by controlling the sigma
36:34 . So this is a sigma factor controls expression of those Heat shot
36:38 Okay. And so it's called P. O. H. Is
36:41 gene sigma H is the name of factor. And so this is gonna
36:47 a example of post transcription of control we're already dealing with the fully formed
36:56 . Okay, this is opposed transcription control mechanism. And so um so
37:02 the question is is this going to translated or not? Okay, It
37:08 to do with the secondary structure that . Okay, so in at room
37:14 30° so you know Uh less than shot temperature. So 30° um the
37:23 secondary structure covers up the river zone sites. Remember there's a ribosome binding
37:28 in the transcript that allows the option bind and translate the transcript. So
37:34 so that represent binding site is covered by the secondary structure that only occurs
37:39 this I mean this is at below temperature that causes the heat shock
37:46 Okay. Which is what you Right? You wouldn't want this expressing
37:49 shock genes that there's no heat Okay, so um now uh like
37:55 said these bindings are never irreversible. it's gonna be a little bit,
37:59 little bit at a time when that actually will Come apart and be translated
38:04 Albeit three light slightly. Okay, you do have proteins that can degrade
38:10 if that happens because again, you want to express the signal factor expressed
38:15 those jeans unless you're in the heat stress situation. So they kind of
38:20 rid of any extraneous sigma factors that produced at normal temp. You have
38:26 that can degrade it. Okay. in this case they called DNA J
38:31 R P E D N A Uh Now in heat stress, the
38:37 here is 42 degrees. Um the and of course is there's not that
38:44 structure present and arrivals on binding site free to be bound. Right?
38:49 you see there the loop here. loops but no loops here. Okay
38:53 so now you get uh the full of translation of the transcript producing sigma
38:59 which will then guide the preliminaries to heat shock genes, promoter of the
39:04 shock genes. Okay, and so produce these proteins that serve also as
39:11 to bind to proteins that are becoming in this, in this heat Conditions
39:19 And they have served to help maintain of those proteins. Okay, so
39:24 proteins themselves that are doing the The chaperone proteins certainly must have some
39:29 of heat resistance to them obviously because able to function at this elevated temp
39:34 their function again, just to bind proteins that don't do so well from
39:39 high temps. And so by trying keep them folded together, they can
39:43 maintain function. And again, the here is yeah, we're elevated temp
39:49 presumably it's not gonna be a long condition. Obviously, if we keep
39:53 this temperature for extended period of it's not gonna matter. You
39:56 how much she heat chucked gene you get too high attempt for too
40:02 , It's just not gonna work. if it's, you know, it
40:05 say in a relatively short time frame it then it can work and some
40:11 may survive. Okay? Uh and only survive, you kind of can
40:15 keep these proteins together functioning in this . Okay, so but again,
40:21 temp. Um and the uh this what will occur. And so then
40:27 as we go back to if it back to normal temperature then this transcript
40:32 then come back to this shape here you'll have minimal expression of the single
40:36 . But it's kind of temperature. kind of what's controlling is really the
40:41 was controlling somewhat the expression. But it's it's controlling a transcript right?
40:47 we get secondary structure or not to drivers and binding site on our transcript
40:55 a sigma factor. So because of its transcription post post transcription control but
41:03 kind of is a obviously playing a , huge, huge influence here.
41:09 . Um is I forgot that Any questions about that. Yeah.
41:16 yeah, the signal factor is inactive it's in this the transcript for the
41:29 factor as in that folded folded form the rivals on binding site is within
41:39 , within that site there and its arrivals can't buy into it. So
41:43 not gonna be translated. So in ambient temperature statements colored, it's not
41:51 . And you don't make cigarette What releases the signal factor right?
41:59 it goes into this form which is been linearize compared to the previous
42:06 And so now it's able to be rivals are combined to it, survivors
42:11 the canal buy into it and translate approaching. So combined you combined to
42:20 some binding site on the transcript of sigma factor and then the single factor
42:28 synthesized right here. So now it's that's a protein. Yeah, understand
42:36 how the proteins differ where we Okay every year. Because when the
42:45 the proteins are because the proteins, proteins have dual function in both being
42:50 proteins but also part of the system recognizes proteins that need to be
42:55 There's a whole system for that as and they function in that part
42:59 The proteins that aren't needed. Certain are tagged for destruction when they're no
43:04 needed either because they're just not functioning anymore or what have you. But
43:08 also serve at LV attempt chaperone proteins bind, bind and help maintain shapes
43:15 proteins that are functional. They can't a dual function. It's a system
43:21 called that ubiquity in tagging system, protein is meant for destruction are tagged
43:26 these are the points that go and them up. So they kind of
43:29 a dual function that way. So it's what is it? It's originally
43:36 to the super factor or like what ? The single factor those. So
43:45 , so here's what's going on is . Uh that one. So again
43:49 form here Is not 100% foolproof. be sometimes when that unfolds granted very
43:57 amount of time. But that's an when you can get a little bit
44:00 sigma factor made even at ambient So you don't want that to
44:05 So that's when these guys kick in . Let's degrade our protein degradation function
44:11 that's how it gets rid of Of the minimal. Yeah.
44:16 Yeah. So like I said, I mentioned with lactose, opera,
44:20 opera all the binding these bindings are folding. You'll get part of some
44:26 small bit at the time. It unfold and make a little bit of
44:28 factor and that's how you get rid it. What? What?
44:33 I feel it. Well, they're they're likely to have enzyme activity because
44:38 they're pretty allergic type enzymes. They , they're pretty little activity.
44:44 Mhm. Yeah. Yeah. Right. And yet mr Okay,
44:55 the last bit here is on regulatory is. Okay, so this is
44:58 to be ah probably fall into the of translation translational control. Okay.
45:11 these are names that form will will . They'll have hm Ology too transcripts
45:20 my bonding to the transcripts. They can act as a block from the
45:24 zone able to to translate hence translational . Right? So, small regulatory
45:32 is are widespread throughout precarious. But there's also um many types of these
45:42 RNA molecules in in in other in we have them. Um But we
45:47 many different subcategories of small regulatory S um something some called I think
45:56 don't need to know this. But may you likely will hear about these
45:59 in other courses. Uh hmm. hmm. I RNA I think is
46:04 type nuclear RNA is another type. there's a whole bunch of different types
46:08 nuclear bombs. But again they're all Michaels and here size wise I think
46:11 talking about 100 2 200 nucleotides. relatively small. Okay um and so
46:21 thing about having RNA molecules for controlling is that that's that's what's controlling the
46:29 itself. So you don't have to to extra energy expense to make a
46:33 . Right so the RNA itself is and that is the control molecules.
46:40 so again very efficient. Okay one there's lots of examples. This is
46:45 of staphylococcus aureus, staph aureus is pathogen. Um like many pathogens they
46:54 to express their virulence genes we call use the enabling the cost disease.
47:02 express those at different times so early infection or later infection in the
47:07 And so those genes need to be in terms of time, time wise
47:12 . So one of these, so three is a um small RNA in
47:19 aureus that has this function. Okay it will target particular targets and the
47:25 is based on having hm Ology between two the RNA three and whatever the
47:33 there is. S a one thought what that particular target is. But
47:38 the points and the S. Remember that stands for the Schindel Garneau
47:44 . That's the private zone. This the ribosome binding site. R.
47:48 . S. Okay. And so like oh RNA. Is typically have
47:53 kind of secondary structure that you see . And so uh so what
47:58 Three does it will and this right is the R. N.
48:04 Yeah is this one right here? . The top string. Okay so
48:10 see how it has Hamal aji alright that target RNA. Okay and uh
48:17 covering up of course the arrivals and site covering up the A.
48:21 G. The start code on. so in that in that scenario problems
48:25 won't bind. Okay it can uh some cases induce further degradation. Um
48:33 because remember that ribosomes that aren't there hanging around will eventually be degraded.
48:37 if you're bound up with another molecule not functioning properly then they'll also be
48:42 . So but it is blocking Right? So when you interfere with
48:46 ribosome function that's translational control. Okay so it's been found that these small
48:53 . Can have finally bring functions in uh promoting expression as well as inhibiting
49:02 as we see here. So this not do not um memorize the slide
49:07 just meant to show examples of of ways in which these act. Okay
49:13 here you see uh in this scenario translation. Okay so here's the transcript
49:19 driver's on binding site. And so like the previous example that can bind
49:23 block the binding site or it can translation. Okay so maybe in the
49:31 there's a secondary structure formed that itself around some binding site. The presence
49:37 the small RNA binds to it and releases that negative effect. And so
49:44 it's exposed and can be translated. the opposite effect put ahead on the
49:48 side right. So I can either in some cases it can in some
49:52 you can activate in some cases it activate expression. So um it can
49:59 here now here so again altered activity regulatory protein. So you may have
50:04 regulatory protein bound to Robertson binding site it right now will be translated.
50:10 then here comes a small RNA that specific for the protein and binds to
50:15 . Okay binding up the regulatory protein it can be translated. So the
50:19 here is that you know either by to the transcript directly or by binding
50:23 protein that's inhibiting translation. Um it either activate expression for blocking. Okay
50:31 you can act both ways and so very common uh controlling genes in different
50:36 . The other thing to mention is the small RNA is occur between
50:43 Okay segments between genes. So I that distinction because the last example are
50:49 anti sense and these are actually smack the middle of the gene. It's
50:57 these are occurring outside genes between Sure any questions about that. Yeah
51:06 um so any sense. And so have um made a different picture because
51:14 think I hope it and I'll post upper class you'll have it but in
51:20 hopes of making it more clear because realized it can be kind of a
51:26 thing that you're the control mechanism is within the gene itself. So I
51:31 of want to draw a different little of diagram. Hopefully clear this
51:35 So any sense RNA. So um the the product is the RNA that's
51:43 controlling molecule. So we're not making protein again Um these are a little
51:48 . You can tend to be about or 3000 nucleotides. So they could
51:53 much much larger compared to smaller But again, the thing with them
51:58 they they originate in the protein coding . So let me just show you
52:02 picture instead of the one you Okay, so here is here's a
52:08 of the chromosome. Okay. N. A protein coding gene.
52:13 we've got our, you know, coding and template strand. Right?
52:17 and minus strand. Okay, so that. Okay, will be an
52:25 coronated. Okay. And it will on within the plus strand.
52:35 so so that's the scenario here. and there are I watch it all
52:43 color. At least there are a of genes control this way.
52:49 this could likely be in addition to whole opera on repression mechanism. But
52:55 but there are a number of genes like this. So anyway the anti
52:59 RNA gene is within the protein coding in the plus strand. Okay,
53:06 let's just say here's the scenario we're to carry out normal transcription check.
53:11 alright. Normally transcribe the gene and produce it, you know an RNA
53:18 RNA. Right. Nothing unusual Okay, so that M. RNA
53:24 relationships here. Right. So we the template. All right. And
53:29 produced Plus so that when we've seen before that M RNA is basically an
53:35 copy of the coding strand of Alright. Except the the user substituted
53:44 . Okay, so again, normal . We can translate that into
53:50 There we go. Okay now where's control the control element? Okay,
53:56 this is to be controlled. Um the anti sense RNA will be
54:02 So you see the watch the arrow up over here. Okay. It's
54:08 so so then that can be Okay. And there is our anti
54:15 RNA. Okay so again remember right orient the the relationship to plus.
54:22 , copy that. Okay. And now uh this works because there's Hamal
54:31 of course between between the anti sense and the transcript. Okay and so
54:38 get binding occurring between the two. , so that's the control so what
54:44 turns on expression of the indecency and assume okay that there is a promoter
54:51 with any sense. Alright, that will respond to a particular single molecule
54:57 something that activator that will promote its . Okay. I'm assuming that that's
55:03 going on as well write the book kind of vague about that. Uh
55:06 so um but there has to be that will trigger the expression. There
55:10 to be some sort of a promoter that will trigger expression of that antisense
55:17 but that's how it works. So , it's complementary binding to the transcript
55:22 in that blocks arrival zone from binding like we saw earlier. Okay,
55:28 again, the translational control. Um the but the point here is
55:34 uh to again, like before it's RNA molecule, just a control
55:39 We're not we're not translating into a . That's the that's the thing that
55:44 the job two is that um that sense RNA these only control the product
55:54 the gene they're in. Right, this will only ever control that
56:00 Okay. And nothing else. No transcript. Just that one.
56:05 so uh so again, the whether in that's the gina controls.
56:10 Not necessarily the case for the small . Is that there can be some
56:15 not as much specificity with those but this it's a one for one kind
56:20 thing. Okay. Um they had about that. Yeah. When you
56:26 that is the highest inside the protein Eugene, it's basically just the same
56:33 . Just transcribed RNA rather than Or is that just specific gene?
56:38 a specific gene. That's what they it, a gene at least.
56:44 . No, so not all like can do that. Uh Well I
56:54 you can have you can have genes are going this way and that way
56:58 protein coding regions. It just depends what are the, what are the
57:03 marks? You're starting stop growing and like that promoters at where are your
57:07 transfer for transcription. You can have orientations because you're not making a protein
57:18 to that has to be the component does the control just are in a
57:22 efficient less energy used. Two is specific. It's making the control expression
57:27 that specific genius in. So we're to get out of DNA. RNA
57:34 go yeah. Right. Exactly. . Exactly. Right. Um so
57:53 , so again, translational kind of . So let's look at um one
57:57 here. Okay, um my answer questions. Okay, so uh you
58:11 we talked about all these, we about the types of control. So
58:15 see what remember here. So on third Wednesday. So obviously Wednesday,
58:53 is the end of Unit three. uh what we talked about on Wednesday
58:57 obviously not on this week's exam. so for 23 is the second two
59:04 . So it's the innate immune We'll start with that one Wednesday.
59:17 let's see the majority has it is is not correctly matched. Right?
59:29 phase variation I would say just call is control of um D expression at
59:37 level of D. N. Is control. Okay that's phrase
59:41 So to defend continuation is transcription. it's it's not allowing the not allowing
59:46 preliminaries to transcribe transient response as We're minimizing expression of rebels um RNA
59:56 transcripts uh chuck is post transcription because have the sigma factor RNA. That's
60:01 of temperature controlled let's say. And anti sense RNA because they bind to
60:08 block translation. Yeah, that's it . So we'll see you on
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