what's up P Penguins so today we are going to go and work through um unit six which is on gene expression and regulation um so real quick you're probably wondering well why do I call y'all penguins and why do I do this whole thing with ap biop Penguins um and so the reason why is because penguins are in those nice little tuxedos um and so as Penguins you are now dressed for success and you are ready to rock and roll um so welcome to being an AP biop penguin so in case you don't know which I'm assuming you all do know about these resources um there is Daily Review going on on Instagram at this point um I'm all the way through with unit six um and I start on unit 7 on Monday There's a 374 page review guide that's on Weebly um so if you go to my website apop penguin. we.com there is this huge review guide for you there um I go through uh the entire uh CED where I have I can statements and then I break it down into topic questions um and then from those topic questions I uh have also organized um all of the frqs and all of the released uh multiple choice questions that are in our possession at this point um plus I added just a couple little quick questions for you in there um I also have recorded fq Fridays at the point of this video I have done every single frq I'm going from 2013 to 2023 um minus 2020 um and I've broken down every question I've shown you the exemplars and so those are all on my website ready for you to go so you can go and practice F frqs and then watch that video or you can pause the video answer the question on your own and then immediately check and see if you have that answer right um this weekend I'm going to work through the two that are in the CED and then at that point I'll be done with all the F frqs there's 120 quizzes games that are on my website so you again those are all open and available for you to play at any point um and then there's review PowerPoint so honestly click on the website you will find tons of resources and they are all 100% free for you um So the plan today we're going to go through molecular genetics we'll talk about operons and we'll talk about biotechnology I have couple practice questions I think I have three multiple choice questions and two free responses in here and then I'll open up for any type of questions and answer okay um as I work through this I find that there's like a slight lag um and so if you have a question you're welcome to throw it into the chat over here um but I'm going to kind of keep working through my my presentation but if I can answer your question I'll jump back and do it um in previous sessions I've seen the students will answer each other in that chat and so if you have an answer to what someone else is saying then you're welcome to answer that question for them um so let's get jumping into this right so central dogma so the central dogma states that we go from DNA to RNA to a polypeptide um and so the genetic material being DNA and so if we go through replication okay replication is where we have DNA and we use that DNA to make a copy of itself you can then go from DNA to RNA that a process of transcription Okay then if you go from RNA to a polypeptide we'll say this translation the reason we don't say this is a protein is because there are sometimes where our proteins are made up of multiple polypeptides so the process of the central dogma is making the polypeptide not really making the protein um so examples of different proteins that may have more than one poly peptide so like hemoglobin is made up of four subunits um collagen's made up of three so most of our proteins actually have multiple polypeptides that work together so if you remember back to unit one the levels of folding that ordinary structure was when we had more than one polypeptide that was bonded together through those R groups um so now it is important that we understand that there are some things that violate That central dogma so one of those would be our retroviruses our retroviruses are going to have an RNA genome and so from that RNA genome they have an enzyme called reverse transcriptase well at least HIV does um and that allows it to go through reverse transcription and it can take its RNA genome and then make it into DNA so it uses the RNA as a template it base pairs up to make a RNA DNA kind of um hybrid and then it uses that DNA to make a second DNA strand which then it'll allow itself to insert into the host DNA and that's how HIV actually works is that it inserts itself into your white blood cells and every time you make copies of your white blood cells you make copies of the virus until it then of course exit exits and makes this little viral you know all that fun stuff um and so in terms of replication we have a couple big things to understand number one Weir taking place is different between a ukar and a pro carrot okay remember UK carrots have a nucleus proc carots do not have a nucleus so in terms of UK carots we'll see replication taking place in that nucleus versus in a proar it will take place in that region um which is called that nucleoid okay um the structure of DNA is slightly different so UK carats have multiple strands and it's linear so it's just these long strings of DNA versus the pro carot has a singular circular piece of DNA and when I say single I don't mean that it only has one strand it's still double stranded because by definition DNA is double stranded yes I do know there are some times and some violations of that where some times DNA is single stranded but for the most part DNA is double stranded so when I say single circular I mean that they have one strand and it's I mean they have one DNA double stranded and it's just one circular they have plasmatocyte group so those three things together would be your nuclear otide um and if we didn't have the phosphate is a nucleoside that's why we call it a Denine triphosphate is because the fact that it's the nucleoside of adenine and then the uh actually at ATP is looking at ribos but whatever okay um and then also when we're looking at DNA we have the purines which would be our double shaded ones um so Adine and guanine so you think about like pure silver AG um and then your Pines are going to be your sine and your thyine okay um and so when we kind of think about all of them you remember cut the pyramid so C UT but since DNA doesn't have ursl we just say C in the T and so it's important that we understand that purines have a double ring pames have a single ring um so I tell my students that a big name means that we have a small structure so a single Ring versus a small name of purine has a double ring so that big structure and then it's important to know the double bonds and I actually was discussing this with another teacher like the students don't need to know that well yeah you do it's directly in the CED the curriculum that we follow that you have to know the number of bonds so a and t has two bonds C and G has three bonds and this is the hydrogen bonds um and so the way that I can remember that is that it takes two like basically two lines to make capital T so two for Adine and thyine and then sizing is the third letter in the alphabet so three for the C and so if you can remember that a and t go together and that C and G go together you'd be good um so ways that students can remember that is that apples are in the tree so a andt and then the cars go in the garage um and then when we get into RNA we talk about ursl you could talk about that the apples are under the tree and so there's the A and the U could be together um and so then when we think about the structure we've got a sess to it okay at your five Prime end there's a phosphate you don't really need to know the counting of it um but in case you really really wanted to know um the way that we count around the structure we've got 1 2 3 4 five and you're counting the carbons on it and so on the first carbon we see that you've got your nitrogen's base on the third carbon where the hydroxy group is of that sugar and then on that fifth carbon is where we see the phosphat that's why we say the five Prime n has the phosphate and the thre Prime n has the hydroxy group and that they're going to be anti-parallel okay and so where I have a three prime across from it's going to be a five Prime and when there's a five Prime across from it will be a three prime and that's going to be important when we talk about the way that replication takes place and being able to eliminate some of our answer choices okay um also directionality is important DNA is read three prime to five Prime DNA is made five Prime to three prime I again anti-parallel okay so students trip that up all the time so it's important that we remember that we read 3 to five and we make 5 to three again anti- parallel and so in terms of replication there's a couple different steps and I attempted to make an animation so here I have helicase now I know I already separated them but it's okay so helicase is going to go through and it's going to unwind the DNA strand the way that it unwinds it is that it's going to break the hydrogen bonds that we have in between those nitrogen spaces as we said before um Adine and thyine have two Seine gline have three the way they they could kind of expand this and ask you questions they might ask you about like the melting point so if there's more adenine and thines in a structure a DNA structure it's going to have a lower melting point than if it has more cytosines and guanines okay so after the DNA of course pulls it apart I'm sorry the helicase breaks those hyren bonds and pulls them apart and of course it's not taking the whole strand apart it's only taking a little section um top isas is going to relax that super coil ahead of the replication Fork when I say replication fork I'm just talking about where is the point where they're coming apart okay because it's going to make like a fork in the road almost and so these two strands are together it opens it up and makes that fork that you might see in between there okay so now way Upstream if you think about any time that you take two things that are coiled together and you pull them apart Upstream is going to get super coil and so that's the do of top highas is that it's going to um break the double bond unravel a little bit and it's going to put those back together that phosphor dier linkage Okay so so then we're going to have primase okay so DNA polymerase is unable to start from scratch so it's going to need a primase prim's job is to make a RNA primer so what it's going to go through is it's going to read again three to five it's going to synthesize 5 to three so what does this look like so what we're going to see is we're going to go through and have the base pair right so cytosine and Guan will pair together and again you see s gu P together so the prime is going to go through and it's going to put on that primer okay and so it base pairs up adne thyine cine guanine and it does the same thing here now again since this is RNA we're going to have urell in there instead of um thyine okay um but that will get replaced later on with RNA I'm sorry DNA pulas we come back in and fix that later okay and then next thing will happen since I've got my primer now DNA polymerase can come on and so I just finish this out by having the helicase open up the next part and then polymerase continues on so G polymer's job is to synthesize the D polymer enzymes tell you what they do helicase breaks apart the Helix primase makes a primer DNA polymerase makes a DNA polymer topy sumaras I guess you think about like a spinning of a top but it's going to unwind the the part okay um and so we have these two different strands we've got our leading Strand and we have our lagging strand our leading strand is going to be synthesized continuously toward the replication fork so as I saw said before we're going to have this replication fork okay it's going to be where helic case is pulled apart the two strands okay so the one that's moving towards the replication fork okay so my upper strand the one that was three to five is being synthesized 5 to three going toward that fork now our bottom strand is going to have a three prime end here and the five Prime end there and so it's going to synthesize the opposite direction that is going to be my lagging strand okay and so it's going to move a little bit make the little Strand and then it opens up a little bit more and makes the next Strand and so we're going to see that it's going to have to keep doubling back and synthesizing that strand it's going to keep kind of jumping if you May and that's our lagging strm so since I have these little fragments the first fragment here the second fragment here or in this case on my diagram the first fragment and the second fragment I need ligas to come in so ligase is going to come in and it's going to seal that bond for me okay so then I can make my full strand um so now I see a question came in the chat why are there different melting points depending on which one's bonding it has to do with the number of bonds so Adine and thyine have two hydrogen bonds and so in since if I would to talk about a DNA strand that has multiple addins and thines in it that means there's a whole bunch of just two hydrogen bonds in there and then if I was talk about a different strand that had moreines and guanines that have three bonds between those three hydrogen bonds then that's going to be more hydrogen bonds which is going to allow it to have a higher melting point it requires more energy to break all those hydrogen bonds than it does with the lower one okay um and it does look like that somebody answered it thank you Nisha um I hope I said that right um for answering that question so moving into transcription okay as we said before transcription is where we're going to read the DNA and we'll synthesiz that RN aan okay so again location is important UK carats will have this take place in our nucleus and the pro carats will take place in the nucleoid keeping in mind that is in the cytool right there's no membrane that separates it in a procaryote okay reminders about RNA oh that's a typo that should say RNA I'm so sorry y'all RNA is made up of adenine um osol sosine and guanine it has the pentos sugar of ribos so that is different than D so if we're think about the differences between DNA and Arna um DNA had thyine RNA has a urel DNA had deoxy ribos RNA has ribos so those are big differences we see there okay um so then purine again is adinin and guanines perin and cine and urel um so now that I have them all kind of think about that you would cut the pyramid CU T um help you remember the Pines um and I see the question why can't it go three prime to five Prime this does sound dumb it it is why can't okay so RNA polymerase um is an enzyme and enzymes have active sites and so my only assumption would be that um in order for The Binding of the New Strand it would have to bind a certain way and that way happens to make it make it 5 to three instead of making it 3 to five um okay so excuse me additionally we think of our base paring rules so adenine and thyine if we're thinking about DNA but it's um Adine and osol when we're looking at RNA again two hydrogen bonds sine guanine with three hydrogen bonds there is the same size where we have a five Prime end and a three prime end um in terms of our five Prime is our phosphate three prime is our hydroxy and the directionality is the exact same as the DNA so the way that I explain this to explain this to my students is that it's the same language so if you were to write now write down everything I say I'm speaking in English to you okay and you're going to be writing it down in English okay you're transcribing it in the same language okay so that is the way I explained it so you're going to read the same direction you're going to write the same direction it's the way that English Works um is of course read one way yeah okay and so we need to make sure that we're looking at our template strand okay so there are multiple names that this can be called and in the CED all four names are in there which means that these can be used interchangeably in a question okay they can call this the template strand they can call it the non-coding Strand the minus strand or the anti-sense Strand all four of those terms can be used to describe the template strand the template strand is the one that has three Prime to five Prime that is being red on DNA to synthesize the RNA and when I say that it's being red it's the one that's going to be base pairing up to to make that RNA strand okay so here again we've got my transcription um RNA polymerase is going to be able to separate them and I don't know if you caught that the enzyme we're using here is RNA polymerase we're making a RNA po polymer so we're using RNA polymerase okay so it's going to be able to pull apart it doesn't need any helicase the AR PL is able to separate them in that spot okay so ARL is going to synthesize the MRNA strand um in the 5 to three prime Direction reading that template DNA in a 3 to five as I've already said so AR PL com through and it base pairs it up yes I'm so excited about this animation like I'm proud of myself for this animation I worked really hard on this so it base pairs up anytime that I have an adenine there's going to be a URL but other than that it looks the exact same so a timesaver okay so if you're trying to work through something on the exam and you're like freaking out because you have to a time crunch okay keep in mind mind that your template strand okay sorry I said that wrong the one that you're going to base pair the MRNA that you're making looks just like the one that's not the template strand The non-template Strand okay looks the exact same only difference is that there's a u so if you're needing to quickly look at it and you're need to quickly make that M&R strand just look at the 5 to3 Prime Strand and just separate switch out all the t's for use and you got a new strand you got the right one okay um so when we think about this there's a promoter this is a site where RNA polymerase is going to bind to start transcription okay um and then there's going to be these things called transcription factors which are your activators or your Inhibitors that'll turn on and turn off gen expression so when we looked at cell communication we talked about this transcription Factor we mentioned how um it can go into the nucleus and it can turn on a gene well the way that it does that is it's going to bind to a site which is then going to allow for the RNA polymerase to bind um so I always kind of think about it like a baseball glove um if you're trying to catch a ball you don't want to catch the baseball barehanded you're going to want there to be a little bit extra support um and so the uh activators are going to kind of act as that right our transion factors are going to extend this the region and it's going to draw the RNA polymerize to that site and it gives it nice secure binding so it can then read that DNA to synthesize that RNA strand okay so after we go through this after we've made our RNA well there's slight differences between a Procare and a UK carot a procario doesn't have a nucleus so it's going to immediately start translating as soon soon as we start um transcribing it it's going to start translating it okay versus in a UK carot we can do some stuff to that RNA before we allow it to leave the nucleus um real quick there's a question what's the difference between a promoter and a primer um the promoter is a site on the the DNA it's just like a a certain coding region um and that's where the RNA polymerase is going to bind um versus a primer is just talking about I guess are you like it's something that's going to start something so like a primer will be like the initial like Point um and so like when we're looking at the DNA polymerase we make a strand um that's like a primer so like crystals I don't know if you ever noticed like how a crystal is formed um they put like a piece of sand in there first um and then that sand gets built upon so our primer is what's going to start the synthesis of that DNA strand it's giving something to build off of um versus the promoter is just like a region so I hope that I've explained that for you um okay yeah mutations later on in this and so there's three different things that we're going to see is going to take place with our post transal modifications again this is taking place only in UK carots because of the fact that transcription and translation can take place different regions right transcription will take place in our nucleus versus translation will take place in our cytool um for both well I guess in new cares so first thing's going to happen is we're going to add a five Prime guanine cap okay this signals the start of the transcript okay this is where the ribosome is going to bind is at that five Prime end so I need to put a guanine over here to say hey this is the start of it this also facilitates the export from the nucleus so this is what's going to allow the RNA to leave the nucleus and come out into the SLE where those ribosomes are we're also going to remove introns these introns are going to be intervening sub sequences they're non-coding regions there's Just Junk in there so it's like if you had a textbook or any type of book and there was like chapters three and four are just blank pages that's a way waste of resources to have to sit there and flip through every single page of your book so what we're doing is after we've realized hey there's this part that is blank in here we're going to cut that part out so that you only have the coding region you only have the words in your textbook um and so we're going to cut that out and that's where we get the alternative Jean spicing is that we can cut out different introns and exons during that kind of uh splicing point and then we're going to have a poly tail the poly tail is just a whole bunch of adne that we put at the end of the MRNA and it's designed to decrease the hydrolytic enzymes there's these enzymes that are in our cyol and their job is just to basically cut from that three the three prime end and it makes our strand smaller and so as we're cutting like the functional parts of that protein or the polypeptide um then we're not going to be able to make the correct protein anymore because we're cutting out that coating sequence that made that polypeptide um and so we this kind of prolongs the life of the MRNA so three things that happened we had a five Prime cap we spliced out the intron and we had a polyat tail so in terms of translation translation was that last step when we make the RNA and we're now going to read that RNA and we're going to synthesize a polypeptide um so in proc carots they happen simultaneously while UK carots they add the cap yes so in terms of proc carots versus UK carots um proc carots can um as soon as they are trans done scribing like so they like literally make the first little blit of the RNA the rabone will attach to it and it can start translating it um and so there was a question a couple years ago anq question where they asked the difference between a prar and ukar in terms of the length of a strand and you would say the Strand was the exact same length because it didn't cut out the entron versus a OT did cut out those introns I think that may have been 2018 but I could be wrong about what year it was he so in Translation this is our ribosome our ribosome is made up of our RNA and then it's made up of proteins there's two parts to it we have a large sub and we have a small subunit the large subunit is going to bind to my TRNA my Transfer RNA that is transferring the amino acids to that rabis and then the small subunit is binding to the MRNA so this is actually where the three different types of RNA that we think about and we talk about are all working together so our RNA makes up the ribosome our TRNA is going to bring the amino acids to the ribosome and then the MRNA has the message from the uh DNA and so locations as we said um UK caros this will take place in cyol or the ruffy r and Procare takes place in the cytool and so um just real quick in case you don't know all ribon start out being in the cytool they'll get a message that allows them to move to that ruff r um so we will see ribosomes on the Ruff but they do all start as stolic ribosomes um and so in terms of our translation there are three steps we have initiation elongation and termination initiation is going to start at Aug I don't know where you are but for me school starts in August Aug um and so that kind of helps me remember the start code on is aug you do not have to have them memorize they're going to give you this beautiful chart on your exam and so if you look right here where is it at met a ug we have met which stands for methionine which is an amino acid but it also stands for the starch so the very first amino acid that you're going to have in every single polypeptide is going to be a methine um I did learn a couple years ago when I was doing one of the practice questions they actually do cut that methine off later but in terms of when you're working on the exam Aug is going to be your start and it codes for methionine elongation is we're going to base pair between the TRNA and the MRNA to add each of the amino acids in and don't worry I made an animation for it I'm super excited about it um and then terminations when we reach a stop code on so we'll have uh ug so if you are a ug fan you know University of Georgia you'll know that they are unstoppable W whatever um there's also UAA in UAG again you don't have to have these memorized because they are given to you on the uh code on chart okay and so in terms of translation there are many steps we said we're going to have to have start code on right um so I already I'm going to assume that we're already started on this that we already had the AUG come in and so we're going to talk about how does translation take place right so there's three sites you have the a site oh my gosh the a site the P site and the E site okay so the a site is where we're going to add the amino acid in okay so we're going to have a TRNA that has the amino acid and it's going to come in the anticodon which is going to be on our TRNA is going to base pair up with the codon that's on my Mr name so he be c c u and then C because it will base pair up so if you're trying to figure out where is that on the uh chart okay you're going to look on your code on so G A is right here so that's going to tell me that I have glutamate and so my glutamate is going to be attached that amino acid in case you're trying to figure out how to use this codeon chart your first Bas is going to be over here so this is my first one was G I look down here I find the G so I know I'm in this kind of row right here my second one was an A so I know that I'm in this box right here and then I look for g a which is right here so glutamate um and you can use again this chart is given to you on your um exam I promise okay so we have our anti-codon pairing up with our codon so then what's in the a site shifts over we translocate okay so we shift over from the a site to the P site and so this is where we're going to have our growing polypeptide now the a site's open and another amino acid is going to come in right um so the TRNA again base pairing up I guess I didn't put the uh animation on there to base pair up but so we base her up and we have our sering so um we see ucg make sering and then of course we translocate and when we translocate now we have the thing in the eite so my eite is going to be my empty CRNA ready to exit Okay um and so we see the glutamate and the Serene is going to now be bonded together on that uh P site okay we have our polypeptide um so after that we then shift over again we have another one base pairing and it's going to keep on going through that shifting until we reach the stop coaton so if you see right here I've got um where am I at I guess I just made a stop coat on just to show you a stop coat on um and so at that point a water molecule will come in which will allow our polypeptide to come apart um the whole structure will fall apart um and then we of course have our little polypeptide now of course it would be much longer than that but you get the idea um what are the pro mechanisms in Dean replication um in terms of per Perforating we just see that DNA polymeris is going to be able to kind of check itself um and so we'll see that just like as you're typing along and you make an error if it realizes that it made the error it just backspace a second fixes it and then goes on um DNA per can also check the DNA strand and it notices if there's a mismatch um and which it will then use a nuclease to cut out that segment and then DNA poas will come in and SE and fix that base pairing rules and then we'll see again liase will seal that back together um so you'll kind of see that that will take place uh and you don't need to know the differences between the types of DNA polymerase you just have to know that DNA polymerase doesn't so DNA polymerase changes out the uh RNA Prime primer back into DNA primer um it synthesizes the DNA polymer um it is going to also uh check for the different errors um when do mutations occur um we're going to talk again about mutations we have not talked about mutations yet I explain a little about termination part um and so there isn't a TRNA that's going to come in and bind because of the fact that this is the stop codon instead a release Factor comes in and so when that release Factor comes in that signals for a water molecule to come in and so we know that when you use water we go through hydrolysis hydrolysis will then break that Bond so that water molecule will break the bond that's right here between the TRNA and that polypeptide and so it'll break that Bond using that water molecule which then allows the whole thing to fall apart um DNA pmer one or two or all DNA polymerises um we don't need know the differences between the two so I'm going to be honest with you I don't have them memorize because I haven't really needed to memorize them and since before the like the 2012 curriculum is why I needed to have those known okay so mutations point mutations mutation at one nucleus bace okay so when we think about point mutation we have a mutation in a single point one point okay so we have a silent mutation there's no change in the amino acid AA stands for amino acid in case you're wondering okay so uua and CU CUA are going to code for the exact same amino acid so although there is an error although it's a different in that nucleotide we still code for the exact same um amino acids so you don't notice an error so we call that a silent mutation versus a missense mutation I change from one amino acid to another amino acid so it's like if I instead of talking about I wanted to walk my dog I say that I walked my fish well that doesn't really make sense in that sentence right that's missense instead of a dog it's a fish so you're just like but it's just a changing of one amino acid there which one of me that changes um versus a nonsense is going to be where we have a premature stop okay so I'm telling you a story I tell you all about how my son jumped off the bed and then we had to take him and I just stopped like you don't know where the end of the polypeptide is you don't know where the end of the sentence was going because I just stopped so it's like a premature stop okay so Salin has no change missense has changed from one amino acid to another and the nonsense is just completely to a stop codon okay versus a Fram shift mutation deals with that there is an insertion or a deletion of one or two nucleotides and that causes you to shift the reading frame so instead of saying the cat ran too far I say to well what TAA that doesn't make any sense but what is happening is that I've shifted my reading frame so instead of reading the cat ran too far I shifted by one letter making it to Kaa which hopefully it doesn't say anything bad but whatever okay so if we're talking about an insertion or delici of three nucleotides it's not going to do that because our codons are in groups of three and so I may add one amino acid I may delete one amino acid but it's not going to shift all of those groups of three okay um I was going to say something okay so um when we get farther and we're talking about like clogs and we're talking about unit 7 and talking about differences um the stum mutation is the reason why we're going to say that DNA is more accurate to use than amino acids because DNA is going to show all those Chang versus if I just look at the amino acid I wouldn't pick up these silent mutations because they're the exact same amino acid so we can also have chromosome mutation this has to do with where we rearrange a certain part or change that chromosome number so that's where we have insertions deletions duplications inversions or transtions insertions where we can insert something deletions where we delete something um duplications we make multiple copies that's what's happening with like Huntington's disease that they duplicated that Gene um too many times inversion it comes out it flips over and then pops back in and then trans a it just moves it to another um chromosome which is where Down syndrome sometimes comes from is that there is a kind of a translocation where it takes a portion of chromosome um 21 and puts it on another chromosome I care which one it is maybe 13 maybe 15 it doesn't matter um and then we can also have changes in our chromosome num so like non-disjunction we talked about I believe in unit five um where we saw that you could have like um two of our chromosomes do not segregate during inase which leads you to having an additional ch rosone in one of your gametes and not in the other and be missing a chromosome one of your gametes and then poly means that all of the chromosomes there's a whole another set so like a triploid has three sets of chromosomes a diploid has two sets of chromosomes a tetraploid has four sets of chromosomes so it's just being you have multiple sets um okay what happens if the TN binded is the wrong amino acid for some reason it goes in um so because of the fact that we have that base pairing rules um you're not going to put the wrong amino acid so there is a specific TRNA Amino atilas which is the enzyme that is going to add the TRNA and the amino acid together so there's that specific binding to that active site so you have the correct amino acid put on the correct TRNA and then you're going to see that that TRNA is going to base pair up with our um mRNA so we have the correct basing there to bring that amino acid in if there is an error it's probably just going to take place that one location you made that one Mis functional Pro protein it's not going to have a problem Downstream because of the fact that it was this one time versus errors that we see in our DNA this error right here that we're seeing these were errors that took place in our DNA and so every time I transcribe and translate that Gene I make the same error this same problem is taking place in then so that's why we see that this is a recurring problem um so like thinking about any of those uh chromosomal chromosome but like point mutation diseases um like sickle cell or TXS or one of those it's in the DNA so every protein is formed in uh non-functionally so in terms of operons okay so operons we only find in proc carrots okay so this is the gene regulation we see it's uh because it's very simplified um so we're going to have again the promoter region which is where our RNA polymerase is going to bind we have our operator this is a site where a repressor binds and then of course we have the genes so there's those three things that make up these operons promoter operator and genes okay so I like to think of this like a rare Road Track okay so the promoter region is where we're going to have our train being our RNA polymerase is going to bind okay the operator is going to be a specific site on that train track okay and then of course the train tracks is the DNA and so a repressor would be like a big rock so if my big rock is on top of my train tracks can my train get on the track well no it can't and so this is going to inhibit that train from moving on those tracks it's going to inhibit RNA polymerase from binding it's going to inhibit it from being able to transcribe that Gene so we have two different types of we have repressible operons and we have inducible operons so let's first think about repressible operons the job of a repressible operon is that it's going to be on and it's going to get turned off okay and I know I say on and off 20 million times with this I don't really know any other way to say it so it's going to be on and off for a while and so with this an example of that would be our trip operon um I don't know if they'll use trip operon on your exam um but it's the main example that we usually use the job of it is going to synthesize tryptophane so we find that most of our repressible operons are going to synthesize something okay there's some type of anabolic pathway they're going to synthesize some big thing okay and so we're synthesizing tryptophane well the bacteria eoli lives in your intestines okay and so when you consume something when you eat food right your body breaks down that food and you're releasing out these amino acids specifically tryptophane so if there is tryptophane in your diet and you consume the tryptophane does the Coline need to make that tryptophane well no it doesn't and so that's why we're going to call this repressible upron because if tryptophan's present it's going to turn that upron off why do I need to make something if you already gave it to me being the eoline okay so it starts out being on and the repressor is inactive okay so the repressor is not found to the operator and so we're going to be synthesizing that tryptophane if that trip is present tryptophane is going to bind to the repressor so if tryptophane binds the repressor okay um it's going to activate my repressor my big rock is now there and the repressor binds to the operator so if the repressor is bound to the operator I cannot have RNA polymerase binding and so my operon is now off since trip is there trip BS the repressor right making it so that I'm not going to make any more trip I don't need to make something I already have versus an inducible opon its job is going to be to turn something on we're going to turn the gene on with this so example we have is the Lac Opera these would be our catabolic Pathways okay I'm synthesizing something to break something else down okay so it starts out being off and the repressor is active so that means that my repressor is always bound to my operator it's always there okay and so if lactose is present lactose is going to bind to my repressor to inactivate it it makes it so that it's no longer bound and since it's no longer bound RNA pulas can bind and it synthesizes the enzymes to break down lactose why do I need to make why do I have to break down lactose if lactose isn't there so it waits until the lactose is there before it can do operons are definitely a negative feedback loop both of these are negative feedback loops there's a specific type of positive feedback that takes place with one of them um it's cap I believe there's like something that works with this um that if there is a high amount of um lactose and a low amount of glucose I think is going to try to um benefit on the lactose versus the glucose I truthfully cannot remember that one off top of my head though I'm sorry um okay so these again I don't know which one they're going to give you on the exam um I don't know if they'll even give you lack or trip on the exam they may kind of trip you up by giving you something different um but you just need to make sure that you're following the path and so whenever I have these I just kind of draw myself a picture to kind of think through it okay repressible again think about the word repress turn something off so that means this one will be on and get turned off inducible if you're inducing someone for labor you're trying to get them to have the baby so we're going to turn the gene on right so it turns off it's off and gets turned on okay and so kind of think about these as opposites so biotech is the last thing we have in this one right so there's four different things that are in the standard it's 6.8 in terms of the curriculum um so our first one is gel faces I they haven't released an exam in a couple years but every time that I've seen one they always talk about there's always the jel faces on there okay so what we do with the J frees is you put DNA samples into these little Wells so there's little kind of pockets up here the wells and notice that this is a negative side and this the positive side DNA is negatively charged if you remember that there are all these phosphate groups in it phosphate is negatively charged yeah so you do kind of need to know about functional groups in terms of like remember that kind of stuff um so phosphate is negatively charged making DNA negatively charged so it's going to be kind of drawn to the positive end and so we're going to see that when we turn the electricity on that we're going to be able to separate the DNA based on charge and size and so the longer fragments will stay up here by the well and the smaller fragments are going to go down here at the bottom okay um so it's kind of like thinking about a chain link fence um who's going to be able to get through that chain fence competing between you and like a rabbit well a rabbit's going to be able to go in and out of the holes in the chaining fence versus you kind of get stuck at that fence um and so it's kind of like that where the gell frees the agros gel has all these little pores in it and so bigger fragments can't go as far they kind of get stuck um versus smaller fragments can kind of weave in and out and so what they may ask you to do is compare those banding fragments and kind of determine um somebody's uh trait so like they'll give you someone this homozygous dominant someone's homozygous recessive someone's heterozygous and you'll be able to figure out um the genotypes based on that um they I don't think they've ever asked like a paternity question but they could ask if have a paternity question um because of the fact that half of your genetic material is going to come from each parent um they could ask that kind of thing so you'll just have to be able to read the diagram or be able to kind of expand on that um another thing you might see is that the thickness of the band so if there's a thicker band it means that there's more DNA there versus a thinner band there less the name um we also have PCR PCR is going to be polymerized Chain Reaction so thinking about chain reaction is going to happen one after the other and so we're going to try to make multiple copies of DNA fragments um and so it goes through these three steps of heating cooling and ening okay um so what happens is we heat it up by heating it up it denatures the DNA it pulls them apart into single strands um cooling it down allows for the primers that we've added to the structure okay um to bind to the specific region we want them to bind to and then the aning is where the D polymerase is going to bind and go through it um because of the fact that we keep heating it up and cooling it down heating up and cooling up because it's going to keep taking place over and over inside a thermocycler we're going to have to use a heat resistant uh polymerase that heat resistant polymerase is Tac polymerase it comes from a thermophile so a bacteria that actually lives in very warm conditions it's going to then be able to uh connect that um somebody says can you explain how the length of drian is related to the positive end um it's not that the length is related to the positive end it's that the negative charge of the DNA is drawn toward the positive end um and so we're going to see that these smaller fragments will move farther because they are able to get pulled and they can go in and out of the um pores that are in the agos gel versus the longer fragments they're pulled toward it yes but they get stuck because they can't get in and out of the pores as fast um okay so PCR is going to allow us to make multiple copies all at once um and so if you're trying to amplify your DNA you're trying to make multiple copies that's what you would go through PCR and then usually after PCR we go through the gel um and then we also have a transformation you probably did this lab with your class um in which you're going to go and you put um DNA um into a solution with your bacteria um you then heat chock it so you heat it up a little bit but then you cool right back down um and so that allows basically the membrane to open up a little bit we're just looking at phospholipids they kind of separate a little bit and then this little plasmid can come in um and so then you're going to grow it onto a plate and you're going to try to see which of them kind of grow on that plate um and so when we look at this we're kind of seeing that we're doing kind of selection for them right we're doing um where if there is antibiotic resistant in that plasma they're going to grow in the presence of that um antibiotic and so I've seen questions where like they put um insulin and they put the antibiotic um sorry antibiotic resistance on that plasmid and then they asked like what's the scent that are going to have the highest amount of insulin res of abilities well it's going to have to be the one that has antibiotic in the presence because that's going to be the highest percent yeah both of them that are transformed are going to be able to grow but the one that's only the transformed bacteria will have the highest percent so you have to really read closely into those questions um and then last but not least DNA sequencing I don't really know how they're going to use this on the exam this is just looking at coding um each of the different uh nucleotides so you can actually determine the sequence of those strands um now somebody in the chat ask why don't UK carotic um have an a operum it's just because we're a little bit more complicated um I think I saw today and read it um somebody said that UK carots do have operons it's not tested on the curriculum um but I've never come across a UK carotic example with an operon there may still be them um but the reason why is because our genes are just separated because we independently regulate them all so each of our genes has their own promoter so we would then regulate the multiple gen so like in a pro carot um let's talk about like I don't know the trip operon trip operon has I think three different genes that it's controlling um and so we synthesize those three genes all at once um in a procario versus like in a ukar there' be a promoter in the first Gene UK carot a promoter and the second Gene and then another chromosome a procaryote I'm sorry promoter and the third Gene and so you would have them on three different chromosomes and so we just can regulate them differently anyway so let's look at multiple choice I realize I'm running short on time that means I'm probably not going to hit my one hour mark but I'm going to do my best um so in terms of this DNA replicates each strin of the original DNA molecule is used as a template for the synth of a second complimentary strand which following features most accurately illustrates enzy mediate syntheses of a new DNA replication fork so we think to ourself okay which way do I read the DNA and which way do I synthesize the DNA well D is read 3 to five five and it's synthesized 5 to3 Okay so let's look at our first example my my first example this one is reading 5 to 3 that's not right so then this one okay we reading it 5 to three and we're synthesizing it 3 to five that's not right here let's see so I'm again reading five to three and synthesizing 3 to five That's Not Right But Here look I read it huh here's a 5 to three and here's synthes of the opposite direction okay so what we're seeing is that I'm reading this bottom strand 3 to 5 and making it 5 to 3 here I see that I'm reading 3 to 5 and synthesizing 5 to 3 5: 3 5 to 3 that's my answer and so you really need to kind of look at it um and figure out which of the directionality in addition you can kind of see that this one was antiparallel so this one wouldn't be showing anti- parallel this one wouldn't showing be anti-parallel so this one and this one both showed anti-parallel but you just weren't looking at the Strand moving in the right direction so you kind to really have to look at it um so CLE IA results in a point mutation the HBP gene mutation results in a replacement of amino acid as a hydrophilic R Group amino acid that has a hydrophobic R Group on the exterior so we substituted hydrophilic which is water loving for hydrophobic which is water hating and that's going to cause the shape of my polypeptide to change okay so this mutation most likely will result in Altered what and so we're trying to figure out well why would this mutation lead to a difference and it has to do with the fact that we're not seeing the same bonding okay so properties of molecules a result of abnormal interaction between adjacent molecules so that's talk about coronary structure I have different R groups so different binding that one sounds plausible let's keep looking DNA structure as a result of abnormal hydrogen bonding between nitrogenous bases this time about point mutation and we're looking at a protein and amino acid that's not talking about the DNA structure so that one's out C talks about fatty acid structure and ionic components between fatty acid chains again I'm looking at amino acids which is part of protein so C's also not right protein second structure as a result of ab normal hydrophobic interaction between R groups and the backbone protein wait that sounds really good I like that one H but that one's not right and the reasoning why is because we're trying to they're try they're tripping you up in a way because if you remember the secondary structure was on hydrogen bonding it was on the alpha Helix and the beta pled sheet the tertiary structure is the r groups so here on D they make it sound really good but that's not the answer because secondary structure is is our hydrogen bonding with our backbone and then the r groups is part of our tertiary structure so don't fall in those traps if you find something wrong about answer Choice don't pick it okay and then here we see operons lactose digestion in eoli begins with hydrolysis of the enzyme beta gyas that was definitely miss said the gene encoding beta whatever Lac Z is part of accordin regulated operon containing other genes required for lactose utilization which following correctly depicts the interaction of the lack Opera when lactose is not being utilized so I don't have lactose let's think for a second okay the point of lack Opera is that I need to make the things to break down lactose there is no lactose this is an inducible operon so it's going to have to be off and get turned on so that means that A and C are not right because these are both showing that they're on right these genes are on okay and I want to find something that's off and gets turned on so then that would be B and D these are the only ones that are off right cuz I've got the repressor bound to my operator okay so I can't have RNA pmer spending because they're Bound in the way so I have to think to your lactose it's not being utilized so would I find lactose in the picture well no I wouldn't so that shows me right here that I've got my operator blocking okay because it's an inducible operon and I have no lactose so lactose is not there so I see that my Gene is my operon is off since you car don't have U is there any specific we to know um so in terms of Regulation they're just going to have a sorry let me read the question the person said person said since UK carots don't have operons is there anything specific we need to know about how UK carots regulate protein synthesis for the HP exam um so in terms of Regulation we're just talking about activators and Inhibitors so if there's an activator it means that it's going to bind to activate and turn on that Gene it's going to ask the transcription factor to stimulate the RNA pulas to bind to the promoter and then of course transcribe that Gene um versus if we have like an inhibitor Inhibitors would of course inhibit the RNA polymerase from binding um which would then of course turn off that Gene so here we see 2017 number six we have a common assay in a technique so um real quick I do want to the reason I put this in here is because this is weird this is different this is unique um the first time I ever saw this was when I was grading the or when I like they posted the questions that year in 2017 and i' never heard of this before and so don't get tripped up if they give you something you've never heard about before take a breath take a breather and look for the biology okay you all know this information you all know this content okay um this is not they're not going to give you something you don't know okay they may package it up in some funky crazy way that's going to throw you through a loop but you know the biology so just look past the words you don't know and look at the biology that you do know and make sure that you're answering the questions that you know because they're just asking you the biology okay so common aay is technique used to determine the amount of double strand breaks in DNA or DNA damage in cells the nucleus of an individual cells placed on microscope's SL coated with an agross gel an electric current is applied to the gel that causes DNA to move electropheresis we know electropheresis and the DNA is stain with fuorescent Dy when viewed using microscope undamaged DNA appears at a round shape and the fragments of damaged DNA extend out from the head the tail the length of tail corresponds to the amount of damage in the DNA so here I see I turn on the electr freezes I see that the head is at the negative end and the tail is at the positive end okay and so all I'm seeing is that if there's breaks right I have smaller fragments my smaller fragments will move and separate from a larger fragment that's all I see here that's all that we see with electris there's nothing that we don't know at this point we are good okay so explain the movement of DNA fragments identify one property of DNA and provide reasoning support how the property contributes to the movement during the common assay so what do I know about DNA and why would the DNA be moving so look at the picture I see there's a negative end I see a positive end I know DNA is negatively charged DNA is negatively charged because the phosphate in it is negatively charged there we go negative charge and is being drawn toward that positive end okay that's simple another thing you talk about is the fact that we're looking at that there's these de these breaks in it right so a smaller fragment is going to move toward the positive end faster F than a shorter I'm sorry I said that wrong a shorter fragment will move towards that positive end faster than a longer fragment so DNA can be different sizes and different size fragments are going to move at different rates okay again you know the biology don't let them confuse you with an example that you've never seen before that's okay they want you to see can you apply your science knowledge okay which you do know you can apply that science knowledge you know this information okay so then Part B in a different experiment cells are treated with a chemical mutagen that causes only nucleotide substitutions so substitution isn't breaking anything right all we're doing is substituting one one nucleotide for another nucleotide is is you know this okay don't get confused predict the likely effects of the common assay for this treatment okay so un damaged DNA will appear as a round shape and fragments of damaged DNA will extend from the head and make a tail well did I damage the DNA nope all I did was change one nucleotide for another nucleotide so I would expect there to just be a head so head only or a head with no tail or you could talk about that the tail would be shorter than one that had double stranded brakes okay so again don't let them confus you so here I have another one and I kind of used this one more because I wanted us to look at um different experimental design components and it did have to do with genes so whatever common bed bug is a species of insect that becoming increasingly resistant to insecticides bed bugs possess several genes suspect of contributing to resistance including p450 abc8 and CPS to investigate the roles of these genes in the insecticide resistance researchers deleted one or more of these genes in different strains of bed bugs as indicated figure one and treated the strains with the insect aside beta whatever each strain was genetically identical except for the deleted Gene and was equally fit in the absence of it the percent survival of each Trin following the treatment is shown in figure one so here I have that figure right I can see the survival of them I can see which ones they have right so if they have the gene or don't have the gene there's a negative if they don't have the Gene and those a positive if they do have that Gene and so the first says Identify the control strain in this experiment so my control strain my control strain is going to be the one that I'm going to be comparing all the treatments against and so since I'm testing how these genes are being affected right so I'm going to test if I don't have those genes that tells me that my wild type my uh strain one is going to be the one that has all those genes and I'm going to be comparing the treatment against that and so that's going to be my control then it says to use the means and confidence intervals in figure one to identify the claim that abc8 is effective at providing resistance to it okay so in order to be resistant to it I need to find that there is a high percent of survival okay so what am I going to compare one two that would allow me to say whether or not abc8 is affected so let's just look at abc8 so here's abc8 one has it two has it three and five do not have it and then four does have it okay but I need to have something that I can compare so if I compare one and three together that would allow me to see that if only ABC 8 was missing would I find that they are going to be resistant and so you can see here okay that their uh what's called their means do not overlap right and then their a bars don't overlap so the reason I really Drew this out here was just so we can kind of compare it to see what happened so every single time that we were missing it so you can kind of see that both these air bars are missing so the air bars of strain one do not overlap with strain three or the mean p survival of strain three Falls outside the 95% confidence interval of strain one strain three shows a significantly significant difference from train one so they needed you to look at the means and the confidence intervals and so when you're saying the air bars do not overlap be very specific about which ones you're talking about you were talking about strains one and three strains one and three the air bars do not overlap and the mean is lower when we see our percent survival with three when it's missing the gene than when it does have the gene be very specific about which ones you're talking about Part B p450 encodes an enzyme that detoxifies insecticides okay so p450 is going to detoxify the insect side abc8 encodes a transport transporter protein that pumps insides out of the cells so this means that the incde gets in but abc8 pumps it back out so just gets it back out of my cell CP s is going to encode an external structural protein located on the exoskeleton that greatly reduces the absorption of insecticides so this means that the insecticide is not going to get into my um my insect based on this information in the data in figure one explain how a deletion of both 450 P 458 um and abc8 results in lower survival compared to deletion of CPS alone okay so 450 and abc8 their jobs are going to detoxify and then also transport the insect side back out okay so it gets rid of it and it also get eliminates it versus CPS is only going to stop you from getting it so if I look at this where I don't have 450 and I don't have abc8 I can see I'm significantly lower right and so we're going to see that when it's deleted and CPS is present the bed bugs cannot detoxify or pump out the incde and so there's a lower bed bug survival okay so because of that then if I look here at four I can see that only CPS was deleted and so I can see that well we're still seeing that that okay so let's set our my wraptor on this I'm inhibiting the amount that comes in but if I if it does come in I'm still able to pump it out and I'm able to get rid of it and so you can see that those are President I deleted and then of course they can detoxify and pump out the inside so there's a higher chance of the survival so you really kind of have to apply what you're seeing in your prompt to your question so I hope that was helpful um I know that there's a lag between when y'all see things and when I say things as well as there's a lag between when I cut the video like it doesn't cut some stuff um so I do have a little moment where you can um write your Q&A in so if there's any questions you have I'm more or less just killing time right now trying to let you catch up and have a time to write your question um and then so I'm just Runing you don't forget um Instagram a AP biop Penguins I've been posting review um I have units seven and unit8 to go um I have Tik Tok who really knows about that we don't really need that right now and of course you already know about YouTube because we're here and you're currently watching this video so you already know about YouTube um so do we need to know a lot about dnamethylation and the other types of Regulation or mostly just oper runs um you could also talk think about like the regulation um so thinking about like that we have methylation the methylation is going to um cause your DNA strand to get um super coiled And So It causes the DNA to wrap tighter um actually wait I lied methylation is going to inhibit the ability for RNA polymerase for binding to it um vers and it also kind of super coils it and then if we acetate it it's going to you're acetylating the tail on the hisone which allows it to unravel slightly um a lot of those you might see a little bit um can you explain how UK carels regulate gen expression if they don't have operons um so it's just having to do with activators and Inhibitors activators are going to bind to specific sites to allow for RNA P Ras to bind versus Inhibitors are going to um block The Binding of that RNA P Ras it's going to make it so it's not going to be able to do it um how much do we need know about operons um it's in the standards there's nearly no way to know which questions they're going to put on the exam what time is next week's unit 7 review unit 7 review I don't think is for another like two or three weeks um I think that because unit 7 is a beast of a unit it's got like 13 Topics in it um so I don't think we have that one until like two weeks from now um so next week we're off the following week we're off and so the following so three weeks from now is when we'll do unit 7's review if you go to my Instagram um like the second pinned page shows you the calendar and it'll show you like what days we're doing the review um but the review is usually at 3:00 on Saturdays um I was on spring break which is why we had to do this one a little late explain transcription factors how they relate to regulation transcription factor is just an inhibitor or an activator that's turning on and turning off a it just binds to a location on the DNA um that allows the RNA Plumas to come to the promoter like that's I think we put a lot of emphasis on it and we freak out a little bit um anytime I've ever seen it on the exam there's been a picture um that kind of shows it to you um so how many hours should you study each day up until the exam so we're currently filming this on April 6th um and so um I would be spending at this point depending on how many APS you have um I would be spending like 30 minutes to 45 minutes um during the month of April and then I would kick set up to an hour when you got into May um because of the fact that you're going to need to start doing um frq practices and you're have to do multiple choice practices and so those be taking a little bit longer um so at this point you're doing a little bit of content review um we have exactly 40 days to the exam starting today so that means you could spend five um days per unit to get through to the exam you could also probably do two units a week um to get yourself to the exam um so kind of create a calendar yourself if you go to Marco learning um I've got a uh study guide posted up there for you um as well as I have um different guid that every we get closer and closer to the exam I keep posting different ones because we all hit that I'm going to study mode at different times um unit 5 through 7 Exam on Monday which you should focus the most that is a question for your teacher I do not know what your teacher is going to focus mostly on um I would F that's a weird unit to have five through seven that's a lot I don't know anyways so are there any other question we have about unit six which is what this review today was on so going once going twice anyways hope that today was helpful remember AP biopan was a just success have a wonderful day bye y'all killing time killing time