AP Biology Unit 4 Exam Review Guide

If you're feeling overwhelmed and exhausted by the intensity of AP Bio as you prepare for the AP Bio exam or a Unit 4 test, don't worry, you've come to the right place. In this video, we'll be reviewing all of Unit 4. That includes 1. Cell communication, cell signaling, and signal transduction. 2. Feedback and homeostasis. 3. Cell division and the cell cycle. And 4. Cell cycle regulation. Cancer and apoptosis. I'm Glenn Wolkenfeld, also known as Mr. W. I'm a retired AP Biology teacher and I love teaching B-I-O-L-O-G-Y. During the decades that I spent in the classroom, most of my students got fours and fives on the AP Bio exam and I think I can do the same for you. As I'll explain in more detail later, if you really want to crush it on the AP Bio exam, you've got to interact with the material and you've got to get feedback. and that's why we created the learn-biology.com website and the BioMania AP Bio app. They're your keys to success on the AP Bio exam. To prepare for this video, I drew upon my decades of experience in the classroom and also carefully analyzed the college board's objectives. As part of that process, I took those objectives and put them into a student-friendly guide for AP Bio, and you can download it. The link is below. Topics 4.1 to 4.4. Part one, cell signaling, the big picture. Cells are constantly communicating with one another. It's a basic feature of life. Cells are never really on their own. They're always in populations or they're in multicellular organisms. So there's direct cell-to-cell communication that you see here where there's some kind of junction between two adjacent cells and molecules can pass between those two cells and that enables one cell to change the behavior of the other. There's also communication that happens through signals. So here you have a cell that's producing a molecule. It's secreting that molecule into the bloodstream or into the extracellular fluid and that message is going to be picked up by a target cell. These signals are known as ligands and there are basically two kinds. If the ligand, the signal, is traveling a long distance through the bloodstream from a gland to another part of the body, that's called a hormone. When cells are in relatively close proximity to one another, they produce local regulators, and that's for short-distance cell-to-cell communication. What are ligands? Ligands are signaling molecules. Many ligands are hormones, and we'll discuss some in depth in this review. What they do is they bind with receptors based on complementary shape, and here I've represented that very simply with a kind of circle and an arc. But because this is biology, you know that the shapes will be extraordinarily complex, like enzymes and substrates. Binding leads to a cellular response, and the mechanism by which that happens is going to be most of what we're going to talk about in this video. What is quorum sensing? This is a kind of cell communication that's seen in biofilm formation in bacteria, and if this seems out of context, these are films that can form, for example, on your teeth, leading to the buildup of plaque. What happens is that bacteria, so here's a single cell, be like one of these over here, what they do is they release signaling molecules shown over here at number two, and those bind to cytoplasmic receptors. So those are receptors that are actually inside the cell, they're not on the membrane surface, when the signal exceeds a certain intensity. So when there's a lot of cells around, that's a quorum, and those signals will be binding with the receptors, and that will activate genes. And that gene activation would lead to the expression of, for example, in this case, it looks like what these cells are doing is they're producing a biofilm, a polysaccharide that forms that biofilm. What's the takeaway? Twofold. The first is that all cells communicate, even bacteria. And the second is that you should brush your teeth so that you don't get a buildup of biofilm leading to plaque. Cell signaling involves three phases. List them. The three phases are reception of a ligand. that's what's happening over here. There's signal transduction where the initial message gets changed into another kind of message that can go into the cytoplasm that often involves amplification of the signal and finally there's a cellular response. We're now going to expand on the material in the previous slide. What happens during the reception phase of cell signaling? The signal molecule, also called a ligand as we've talked about before, binds with a receptor molecule. Here you can see a receptor that has a more realistic depiction and you can see how it's embedded in the phospholipid bilayer of cell membrane. That binding is based on complementary shape. What happens during the transduction and response phases of cell signaling? The receptor during the transduction phase interacts with membrane protein. to produce a second messenger. So something will be happening between here and other proteins in the membrane to bring about this second messenger. The second messenger with other relay molecules will bring that message to the cytoplasm. activating enzymes, or the nucleus where we'll have the activation of genes. How is the mechanism of steroid nonpolar hormones different from that of water-soluble hormones? The hormones we've talked about so far, the cell communication mechanisms we've talked about, have all involved water-soluble hormones. But what if the hormone is nonpolar, a steroid hormone like estrogen or testosterone? In that case, these hormones, which are nonpolar, can diffuse. through the phospholipid bilayer. And once they're there, they can bind with a cytoplasmic receptor. That forms a receptor hormone complex, and that is capable of diffusing into the nucleus, where it acts as a transcription factor, something we'll talk about in AP Bio Unit 6. But all you need to know for now is that that can activate genes. So the DNA gets made into RNA. The RNA goes into the cytoplasm. It gets read by a ribosome and gets made into a protein. protein. Water-soluble hormones, they're capable of binding with receptors, they interact with second messengers, and they bring about a cellular response. And in general, these responses are slower but more longer lasting. These responses are quicker. Topics 4.1 to 4.4 part 2. Now that we've had an overview of cell communication, we're going to look in depth at an illustrative example at epinephrine, and G-protein coupled receptor systems. Before we delve into this, I want to let you know that I have a song that's a rap about cell communication, which covers much of this material. The context for what we're about to review or learn is the fight or flight response, and that has effects throughout our bodies. One of the effects is the effect on the adrenal glands, which produce a horn. hormone that's called epinephrine or adrenaline, and that acts upon the liver to get it to produce glucose that goes into the blood as part of the fight or flight response. Epinephrine is also known as adrenaline. It's a polar water-soluble hormone. You can see these hydroxyl groups over here and over here. Here's an amino group. This is not going to be able to diffuse into the cytoplasm. It's going to bind at the membrane. Note that epinephrine's effects are widespread. but tissue specific. So epinephrine is going to get released from the adrenal glands into the bloodstream. It's going to go everywhere. It's going to touch every cell in your body, but only tissues with receptors are going to respond. That response will differ based on tissue types. So all of these are adaptations that are part of the fight or flight response. So over here will decrease digestion because when you're trying to fight off some mortal threat, you don't need to be digested. at that moment. You want to increase your heart rate so that you can deliver more food and oxygen to your cells. Pupil dilation, more light, you're going to have better senses. Conversion of glycogen to glucose, that gives your cells, your muscle tissue, more energy to fight or flee. Bronchial dilation allows you to get more oxygen into your lungs so you can deliver more oxygen to the cells of the body. Epinephrine interacts with cells in the liver and it induces changes that cause causes those liver cells to take stored glycogen, that's a polysaccharide, and to hydrolyze it into the monomers of polysaccharide glucose. That glucose then diffuses into the bloodstream, and there it goes to the muscles of the body and to other organs as well. And that provides energy to fight or flee as part of the fight or flight response. The question for us is, how does epinephrine get liver cells to bring about this response? So we're now looking... at the off state before epinephrine is released and in this moment the receptor is unbound there's no epinephrine in the system there's a nearby membrane protein that's called a g protein a g protein is not a receptor it's a membrane embedded protein and it can oscillate between two states now it's off it's inactive nearby the g protein is a membrane embedded enzyme not a receptor but an enzyme that's called adenaline. cyclase that is actually the correct pronunciation and it's also in the off state and as a result it's not activating the second messenger what happens when epinephrine enters the system first thing that happens is that epinephrine binds with a G protein coupled receptor. So here's epinephrine, and here it's binding with the receptor. This is a complicated protein, and we've talked about allosteric shifts in relationship to enzymes where where when something binds at an allosteric site, it can then change the active site. Well, the same mechanism is at work here. Epinephrine's binding over here, and that change kind of ripples through this protein and it induces a change over here. Now, right at this moment, the nearby G protein is still dormant. It's still bound to GDP. GDP is a relative of ADP, and it's the low energy form. It can oscillate. between this low energy form and a high energy form that we're going to see in a minute and that happens when the G protein becomes activated. What's the effect on the G protein of epinephrine binding with the receptor? Well the G protein is then able to interact with the receptor. We noted before that the receptor has changed on its cytoplasmic side and that enables the G protein to interact with that part of the receptor and that causes the G protein to discharge GDP that's the low energy form and to bind with GTP that's the high energy form and again notice that this has three phosphates over here just like ATP this only has two phosphates over here like a DP the result is that the G protein now becomes activated so what happens to the G protein once it's bound with GTP it drifts in the membrane it ultimately binds with adenylal cyclase, this membrane-embedded enzyme. That activates adenylal cyclase. And adenylal cyclase's substrate is ATP, and it converts it into a molecule called cyclic AMP, which is the second messenger in these G-protein coupled receptor systems. Note that ATP is triply phosphorylated. This only has one phosphate, and the AMP stands for adenosine. monosine mono, mono as in one, phosphate. What have we done? We've taken our initial messenger and we've transduced it, creating the second messenger. So let's review what we've talked about so far. We've talked about reception. We have the ligand, which is epinephrine. It binds with the G protein coupled receptor. The receptor changes shape on its cytoplasmic side. It interacts with the G protein, causing it to discharge DDP. which is what it's bound to when it's dormant and bind with GTP which is what it binds with when it's active. The G protein then in turn can activate adenylal cyclase which takes its substrate ATP and converts it into cyclic AMP, the second messenger. What we're going to look at next is the cellular response. The second messenger, cyclic AMP, is going to activate a chain of relay molecules. These are called kinase. or kinases. And this activation involves one kinase activating the next kinase activating the next. I've only put three in this chain, but there can be many, many more, and that's called a phosphorylation cascade. How does that phosphorylation cascade work? The kinases are activated by phosphorylation, by gaining a phosphate. And once they're activated, what they do is they activate the next kinase in the chain. So here Here we have protein kinase one that acts upon protein kinase two by phosphorylating it. So now protein kinase two is active, phosphorylated. What does it do? It activates protein kinase three by phosphorylating it. I've only shown three, but there can be many more in this chain. And we get this domino-like effect of one kinase activating the next and activating the next. Once we get to adenylal cyclase then each step involves multiple activations. Adenylal cyclase will activate many cyclic AMPs. Each of these cyclic AMPs will start different phosphorylation chains and the result is signal amplification. We had one epinephrine enter the system but by the end and I couldn't of course depict that here but you'll have the activation of millions of enzymes to bring about a massive cellular response. In the case of liver cells, and the way that they're acted upon by epinephrine, the response is activation of the terminal enzyme, which is glycogen phosphorylase. And what glycogen phosphorylase does is it converts glycogen, again, a polysaccharide. into glucose, a monosaccharide, that glucose diffuses into the blood, giving you energy for the fight-or-flight response. Are you asking yourself, how am I going to get a 4 or a 5 on the AP bio exam? It's a a good question because it's a hard test but we have a plan for your success go to learn-biology.com sign up for a free trial and complete our interactive tutorials and interactive ap bio exam reviews we guarantee you a four or five on the ap bio exam see you on learn-biology.com topic 4.5 feedback and homeostasis what is homeostasis what are feedback mechanisms and how do they to homeostasis. Homeostasis is the tendency of a living system to maintain its internal conditions at a relatively constant optimal level. Your body temperature, for example, stays around 37 degrees Celsius 98.6 Fahrenheit despite fluctuations in the external temperature. The changes in your body to maintain that temperature, that's a great example of homeostasis. Feedback is when the output of a system is also an input. So here we have some system, here's the thing that's coming out, and feedback is when it feeds back into the system. So the output is also an input. And feedback can do two things. One is connected to homeostasis. It can allow organisms to maintain homeostasis as they respond to internal and external changes, just as I told you with temperature. Or it can accelerate internal changes and drive a process towards a conclusion. This is generally connected with what's called negative feedback, and this is connected with what's called positive feedback. Let's talk about set points. What is a set point? How are set points used in negative feedback? First, a word about the method here. We're going to talk about this in relationship to your home heating and cooling system. It's much easier to understand this before we look at the biological examples. So a set point is where you set the thermostat. It's the value around which. which a homeostatic process fluctuates. So above, the set point for the thermostat is 68 degrees Fahrenheit. In negative feedback, the output of the system feeds back to the system in a way that decreases the system's output. So here we have the set point. Here's a measurement of the temperature. The set point is above the temperature. That'll send a signal to turn on the furnace. That'll generate heat. Heat feeds back to the system. There's a thermostat over here with a thermometer that will increase the temperature and then when we get to 68 degrees Fahrenheit, the set point, the system will turn off. Negative feedback promotes homeostasis, returning a system to its set point. How can antagonistic negative feedback loops be paired to promote homeostasis? So, same goal, keep the temperature at 68 degrees. Well, here we have a negative feedback system that responds when conditions are are above the set point. So temperature 70, the set point is 68. What will you do? You'll have a signal that turns on an air conditioner that will put out cool. It's a real word. And that will feed back to the system. And eventually it'll get the system to turn itself off. There's been cooling and we've therefore lowered the temperature. But we still have a heating system. And if the temperature goes below the set point, then that's that system would turn on, it would release heat, that would feed back to the system and that would wind up turning the system off. So we have paired antagonistic systems, one for cooling, one for heating. Now we're gonna look at some biology. Let's talk about how feedback works in blood sugar homeostasis. It's important to your body to maintain your blood sugar levels, your blood glucose levels. The main hormone that controls that is insulin and it's a negative feedback system. And response. to high blood glucose levels after eating a sugary or a starchy meal, your pancreas will release the hormone insulin, just represented here as a triangle. In the liver, insulin will bind at a receptor over here, and that will unleash a signaling cascade, and that talks to a glucose transporter. That's a channel that allows for facilitated diffusion. If glucose is in higher concentration outside, then inside the cell, it'll... diffuse into liver cells and the glucose will get converted into glycogen, which is a storage polysaccharide, or it'll get converted into fat. Blood glucose levels down, homeostasis restored. But as with our home heating and cooling system, insulin is paired with another hormone. So let's explain how insulin and glucagon maintain blood glucose homeostasis. Our blood glucose has a set point about 90 milligrams per hour. per deciliter. Above the set point, the pancreas will release insulin. Eat a big meal, insulin gets released, and your liver, fat, and muscle cells, which aren't shown, will absorb glucose and store it away as glycogen. Below the set point, that's when you've gone a little while without eating, what'll happen is that the pancreas will release a second hormone called glucagon, and that will induce the liver to convert its stores of glycogen. into glucose. Glucose goes into the blood, homeostasis is restored. An important AP bio skill is explaining what happens when systems get disrupted. And here we're going to explain how blood glucose homeostasis breaks down in type 2 diabetes. That's also called adult onset diabetes, but increasingly it's happening in teens and even children due to the obesity epidemic in the United States. We're going to look at normal metabolism first, which we just discussed. Here we see insulin in response to a high blood glucose level is binding with the insulin receptor. There's a signaling cascade that causes the glucose channel to open. There's glucose absorption into the cells, blood glucose level falls, homeostasis restored. In people with type 2 diabetes, what happens is that the cells become insulin resistant. There's glucose in the blood, there's insulin released from the pancreas, but the binding... of insulin does not lead to the signaling cascade and because of that the glucose channel remains closed because of that blood glucose level stays high and that damages organs and tissues breakdown of homeostasis leading to type 2 diabetes we just discussed adult onset type 2 diabetes how does that compare with type 1 diabetes type 1 is also known as juvenile diabetes It's an autoimmune disorder, and basically what happens is that cells of your immune system attack the pancreas cells that produce insulin. Therefore, those cells can no longer secrete insulin, and therefore, even in response to a high blood glucose level, insulin is not secreted. That can only be treated by insulin injections. Type 2 diabetes we've just discussed, also called adult onset, and that involves insulin resistance where the receptor is become. insensitive to the insulin signal. All of the biological feedback loops that we've talked about so far relating to blood sugar have involved negative feedback loops. What about positive feedback loops? How does positive feedback work? Explain how positive feedback works during childbirth. So in positive feedback, the output of a system feeds back into the system, increasing the system's activity and output. It doesn't involve quieting that leads to homeostasis. It involves acceleration. It drives a biological process such as childbirth to a conclusion after which the system shuts down. In childbirth the growth of a baby activates uterine stretch receptors. The uterus among other things is a big muscle and that muscle is stretched out. It sends messages to the brain. The brain releases oxytocin, a hormone. That oxytocin then circulates in the blood when it's picked up by receptors in uterine cells that leads to more contraction. That increased contraction leads to more oxytocin release, and ultimately that continues until the baby is born. Explain how feedback leads to fruit ripening. If you were to pause the video and take a look at this diagram, I'll bet you that you could figure it out. This is a positive feedback system. Ripening in fruit leads to the release of a hormone that is a gas. It's called ethylene. Ethylene receptors in nearby fruit pick up the ethylene and that induces additional ripening and more ethylene production. That increased concentration of ethylene accelerates the ripening process in all the fruit, leading to more ethylene. So eventually all the fruit ripens. In fruit shipping, you can prevent that by pumping carbon dioxide into the storage container where the fruit are and that suppresses the ethylene and that's how you can ship fruit longer. distances. If you want Watching this video, you're probably wondering, how am I going to get an A in my class and a 4 or a 5 on the AP Bio exam? At Learn-Biology.com, we understand why students struggle with AP Bio. The material is complex. is brutal and the vocabulary is ridiculous AP bio is hard it's easy to feel overwhelmed and inadequate to get that a or that four or five you need an easier way to study and that's why we cre Learn-Biology.com. It's an interactive AP bio curriculum with tutorials that have quizzes, flashcards, and interactive diagrams that give you the feedback that you need so that your confidence soars and that you can easily get A's on your tests and a 4 or a 5 on the AP bio exam. We have comprehensive AP exam reviews and a subscription comes with a money-back guarantee. If you do the work, you'll succeed. I guarantee it. So here's your plan. Sign up for a free trial subscription at learn-biology.com, complete our unit reviews, and get ready to crush the AP bio exam. You do not want to end the year with regrets. Learn-biology.com, your key to AP bio success. Topic 4.6, the cell cycle. On a big picture level, what does mitosis do? List three of its key functions in living things. Note for this question that mitosis as it often is, is synonymous with eukaryotic cell division. Mitosis duplicates the chromosomes of a eukaryotic cell, transmitting that cell's entire genome to its daughter cell. So here you have the parent cell, it's got two chromosomes. Here those chromosomes have been duplicated, now they're being pulled apart, and now you have daughter cells, each with two chromosomes, and each one is going to be an exact clone of its parent cell. parent cell. In a multicellular organism like you and me, mitosis is how an organism grows and repairs itself. Remember that you started life, as all multicellular beings do, as a single cell. In a unicellular eukaryote, like a paramecium or an amoeba, mitosis is how reproduction occurs. Describe what happens during the cell cycle. The cell cycle, as you can see in this diagram, can be divided into two main phases. So the outside orange part of the circle, that's interphase. This yellow part over here, that's mitosis or M phase represented by the letter M. During interphase, you can subdivide three basic phases, but the cell doesn't appear to be dividing during interphase. The first is G1, and during G1, the cell increases in size. G1 stands for growth phase one. During S, which stands for synthesis, you have DNA replication or chromosome duplication. And during G2, growth phase 2, you have the growth of the structures that are required for cell division. During M phase, you have mitosis, separation of the chromosomes followed by cytokinesis. So at the end, you have two donor cells that are clones of the parent cell. Describe the phases of mitosis. We begin with interphase during which the cell grows and replicates its DNA. During that time, it doesn't look as if it's dividing, but DNA replication, for example, has occurred. During prophase, chromosomes, which are spread out as what's called chromatin during interphase, they condense into these X-like structures. The nuclear membrane disintegrates, and a spindle apparatus, which is these fibers over here, you can see the entire apparatus in the next phase start to grow from each centrosome. During metaphase, the spindle fibers grab onto the chromosomes and they pull and push them to the cell equator. If you can sort of imagine a line running down from top to bottom, that would be the cell equator. I talked about this X-like formation that the chromosomes are in. That's because each chromosome is doubled and consists of two clones called sister chromatids. During anaphase, the spindle pulls the sister chromatids apart and starts dragging them. to the opposite ends of the cell. At the same time, there are what are called non-kinetochore microtubules. A kinetochore is like a handle on the chromosomes that these spindle fibers use to pull the chromosomes apart. But there are other fibers that basically push on one another, and that causes the cell to elongate. During telophase, a new nuclear membrane starts to grow around each set of chromosomes. The chromosomes spread out into their interphase formation. so you can't really see them anymore. And a nucleolus reappears in each cell. It disappeared during interphase. The nucleolus makes ribosomes, and ribosome production shuts down during most of mitosis. Finally, during cytokinesis, the cell splits apart into two daughter cells. I have a great song about mitosis. Mitosis, chromosomal ride, in a chromatic anaphylophase divide. You carry out scope from one cell to two. Mitosis, how cells renew. and I'll put the link below. Explain the importance of the G0 phase of the cell cycle. Basic idea here is that not all cells go through the entire cell cycle. So if you have highly specialized cells, like a nerve cell or a muscle cell, they'll leave the cell cycle and they'll enter into G0 after which they won't divide. Certain stimuli however can induce cells in G0 to re-enter the cell cycle. Topic 4.7, regulation of the cell cycle. Describe the role that checkpoints play in regulating the cell cycle. Cell cycle checkpoints are moments when the cell checks its internal conditions and decides whether to progress to the next phase of the cell cycle. If If certain molecules are in the right concentration, then the cell continues through the cell cycle. And if not, the cell moves into G0 or might initiate what's called apoptosis. We'll explain that in a moment, which is called programmed cell death. The primary checkpoints to know about for AP Bio are the G1 checkpoint over here, the G2 checkpoint, and the M checkpoint. What is apoptosis? I've talked about that several times. I know that. the second p is silent apoptosis is programmed cell death it's part of a signaling cascade that involves the mitochondria and the nucleus it's highly regulated which is very different from cell death that results from traumatic cell injury cells are broken down into cytoplasmic fragments that are called blebs you can see some of those over here and over here and blebs are consumed by cells of the immune system preventing cell cellular debris and enzymes from damaging nearby cells. What are cyclins and cyclin-dependent kinases? Cyclins and cyclin-dependent kinases are important internal regulators of the cell cycle. The cell cycle is regulated by outside signals, but also by internal conditions. Cyclins are molecules whose concentration rises and falls throughout the cell cycle. So like for example, you can see that cyclin E rises. right before the S phase. Cyclin A rises right before G2. The cell has mechanisms to read the level of these cyclin concentrations. Kinases, which we discussed previously in the context of cell communication, those are molecules that activate other molecules often by phosphorylating them. They're not shown. And cyclin-dependent kinases, or CDKs, are kinases that respond to rising and falling levels of cyclin levels. Now we're going to put that all together and see what some of the mechanisms are that regulate cell division. Explain how the interactions between cyclins and cyclin-dependent kinases control the cell cycle. So CDKs, here they are over here, are present at a constant level throughout the cell cycle. By contrast, the level of cyclins that we saw in the previous slide rise and fall. When cyclin levels are high, the cyclins... bind with CDKs to form a complex called maturation promoting factor, but a good way to remember that is just think of it as mitosis promoting factor, because once you have MPF, that allows the cell to pass through the G2 checkpoint and actually divide. During M phase, however, the cyclin is broken down, and that allows the process to repeat in each donor cell when it grows to the appropriate size and gets ready. for cell division. We talked about the cell cycle, now let's talk about dysregulation of the cell cycle. What's the connection between cell division and cancer? What are the two types of genetic mutations that are connected to cancer? Cancer is a disease of unregulated cell division. As opposed to cells staying in place doing what they're supposed to do, they become rogue players pursuing their own destiny at the cost of the organism. Mutations in genes that are called called proto-oncogenes increase cell division by creating too many growth factors. Growth factors are things that stimulate cell division within a cell itself or within other cells. And there are other kinds of genes that are called tumor suppressor genes. And what they do is they remove cell division inhibitors, the kind of checkpoints that we've seen in previous slides. So in normal cells, you have the breaks. Those are tumor suppressors. And you have the accelerator. Those are growth factors, but they act at appropriate times. When cells become cancerous, it can be for one of two or actually both reasons. You can have mutated tumor suppressors. that can't prevent cell division, even when cell division shouldn't be happening. And you have growth factors that promote cell division at unneeded moments. Describe how a mutation in the Ras proto-oncogene can induce a non-cancerous cell to become cancerous. What we're gonna do now is really cool because we're gonna connect what we've learned about the cell cycle and its control to what we learned about previously relating to cell communication. So, Ross is a G protein over here and as a proto-oncogene it only becomes active when an outside growth signal binds with Ross's coupled receptors. So here we have binding that activates Ross, it picks up GTP that sets off a phosphorylation cascade and that leads to cell division. So this is in a healthy normal system. Ross only gets activated when there's a ligand. When ROS becomes cancerous, when it mutates from a proto-oncogene to an oncogene, then it becomes constitutively active. And constitutively means it's part of its nature to be active. Normal ROS is only active, it only binds GTP when the receptor binds a ligand. But this ROS, which is an oncogene, is constitutively active. It's binding GTP even in the absence of a growth signal. And because it's always active, the growth factor over here is overproduced, and that results in too much cell division. This is connected with about 30% of human cancers. Describe how a mutation in a tumor suppressor gene such as p53 can contribute to the development of cancer. P53 is a tumor suppressor gene. When the cells experience DNA damage, a signaling cascade, activates p53. So here we have DNA damage, it's detected, there's a signaling cascade, and now p53 is activated. If the damage can be repaired, then what p53 will do is it'll halt the cell cycle while DNA repair enzymes fix the damage. So we're going to fix up the DNA, that's what's happening over here. If the damage is too great, then p53 will initiate a whole signaling cascade that will cause the cell to initiate apoptosis. So either we have repaired DNA that occurs while the cell cycle is halted or the cell will self-destruct. Cancer has been prevented. If mutations lead p53 to become non-functional, then the cell will continue to divide even with damaged DNA. So here we have DNA damage. It's been detected. but p53 can't do anything about it therefore there's no stop signal the cell will continue to divide and that will increase the chance of the cell acquiring further mutations that can lead it to become cancerous again dysregulation of a signaling cascade dysregulation of a cell cycle repair mechanism leading to cancer here are your next moves on your journey to ap biosuccess number one Go to learn-biology.com, sign up for a free trial of our AP Bio curriculum. We guarantee you're four or five. And then watch this next video.

Cancer and apoptosis. I'm Glenn Wolkenfeld, also known as Mr. W. I'm a retired AP Biology teacher and I love teaching B-I-O-L-O-G-Y. During the decades that I spent in the classroom, most of my students got fours and fives on the AP Bio exam and I think I can do the same for you.

As I'll explain in more detail later, if you really want to crush it on the AP Bio exam, you've got to interact with the material and you've got to get feedback. and that's why we created the learn-biology.com website and the BioMania AP Bio app. They're your keys to success on the AP Bio exam.

To prepare for this video, I drew upon my decades of experience in the classroom and also carefully analyzed the college board's objectives. As part of that process, I took those objectives and put them into a student-friendly guide for AP Bio, and you can download it. The link is below. Topics 4.1 to 4.4.

Part one, cell signaling, the big picture. Cells are constantly communicating with one another. It's a basic feature of life.

Cells are never really on their own. They're always in populations or they're in multicellular organisms. So there's direct cell-to-cell communication that you see here where there's some kind of junction between two adjacent cells and molecules can pass between those two cells and that enables one cell to change the behavior of the other.

There's also communication that happens through signals. So here you have a cell that's producing a molecule. It's secreting that molecule into the bloodstream or into the extracellular fluid and that message is going to be picked up by a target cell. These signals are known as ligands and there are basically two kinds. If the ligand, the signal, is traveling a long distance through the bloodstream from a gland to another part of the body, that's called a hormone.

When cells are in relatively close proximity to one another, they produce local regulators, and that's for short-distance cell-to-cell communication. What are ligands? Ligands are signaling molecules. Many ligands are hormones, and we'll discuss some in depth in this review.

What they do is they bind with receptors based on complementary shape, and here I've represented that very simply with a kind of circle and an arc. But because this is biology, you know that the shapes will be extraordinarily complex, like enzymes and substrates. Binding leads to a cellular response, and the mechanism by which that happens is going to be most of what we're going to talk about in this video.

What is quorum sensing? This is a kind of cell communication that's seen in biofilm formation in bacteria, and if this seems out of context, these are films that can form, for example, on your teeth, leading to the buildup of plaque. What happens is that bacteria, so here's a single cell, be like one of these over here, what they do is they release signaling molecules shown over here at number two, and those bind to cytoplasmic receptors. So those are receptors that are actually inside the cell, they're not on the membrane surface, when the signal exceeds a certain intensity. So when there's a lot of cells around, that's a quorum, and those signals will be binding with the receptors, and that will activate genes.

And that gene activation would lead to the expression of, for example, in this case, it looks like what these cells are doing is they're producing a biofilm, a polysaccharide that forms that biofilm. What's the takeaway? Twofold. The first is that all cells communicate, even bacteria. And the second is that you should brush your teeth so that you don't get a buildup of biofilm leading to plaque.

Cell signaling involves three phases. List them. The three phases are reception of a ligand.

that's what's happening over here. There's signal transduction where the initial message gets changed into another kind of message that can go into the cytoplasm that often involves amplification of the signal and finally there's a cellular response. We're now going to expand on the material in the previous slide. What happens during the reception phase of cell signaling?

The signal molecule, also called a ligand as we've talked about before, binds with a receptor molecule. Here you can see a receptor that has a more realistic depiction and you can see how it's embedded in the phospholipid bilayer of cell membrane. That binding is based on complementary shape. What happens during the transduction and response phases of cell signaling?

The receptor during the transduction phase interacts with membrane protein. to produce a second messenger. So something will be happening between here and other proteins in the membrane to bring about this second messenger. The second messenger with other relay molecules will bring that message to the cytoplasm. activating enzymes, or the nucleus where we'll have the activation of genes.

How is the mechanism of steroid nonpolar hormones different from that of water-soluble hormones? The hormones we've talked about so far, the cell communication mechanisms we've talked about, have all involved water-soluble hormones. But what if the hormone is nonpolar, a steroid hormone like estrogen or testosterone? In that case, these hormones, which are nonpolar, can diffuse. through the phospholipid bilayer.

And once they're there, they can bind with a cytoplasmic receptor. That forms a receptor hormone complex, and that is capable of diffusing into the nucleus, where it acts as a transcription factor, something we'll talk about in AP Bio Unit 6. But all you need to know for now is that that can activate genes. So the DNA gets made into RNA. The RNA goes into the cytoplasm.

It gets read by a ribosome and gets made into a protein. protein. Water-soluble hormones, they're capable of binding with receptors, they interact with second messengers, and they bring about a cellular response.

And in general, these responses are slower but more longer lasting. These responses are quicker. Topics 4.1 to 4.4 part 2. Now that we've had an overview of cell communication, we're going to look in depth at an illustrative example at epinephrine, and G-protein coupled receptor systems.

Before we delve into this, I want to let you know that I have a song that's a rap about cell communication, which covers much of this material. The context for what we're about to review or learn is the fight or flight response, and that has effects throughout our bodies. One of the effects is the effect on the adrenal glands, which produce a horn.

hormone that's called epinephrine or adrenaline, and that acts upon the liver to get it to produce glucose that goes into the blood as part of the fight or flight response. Epinephrine is also known as adrenaline. It's a polar water-soluble hormone. You can see these hydroxyl groups over here and over here. Here's an amino group.

This is not going to be able to diffuse into the cytoplasm. It's going to bind at the membrane. Note that epinephrine's effects are widespread. but tissue specific.

So epinephrine is going to get released from the adrenal glands into the bloodstream. It's going to go everywhere. It's going to touch every cell in your body, but only tissues with receptors are going to respond.

That response will differ based on tissue types. So all of these are adaptations that are part of the fight or flight response. So over here will decrease digestion because when you're trying to fight off some mortal threat, you don't need to be digested.

at that moment. You want to increase your heart rate so that you can deliver more food and oxygen to your cells. Pupil dilation, more light, you're going to have better senses. Conversion of glycogen to glucose, that gives your cells, your muscle tissue, more energy to fight or flee.

Bronchial dilation allows you to get more oxygen into your lungs so you can deliver more oxygen to the cells of the body. Epinephrine interacts with cells in the liver and it induces changes that cause causes those liver cells to take stored glycogen, that's a polysaccharide, and to hydrolyze it into the monomers of polysaccharide glucose. That glucose then diffuses into the bloodstream, and there it goes to the muscles of the body and to other organs as well.

And that provides energy to fight or flee as part of the fight or flight response. The question for us is, how does epinephrine get liver cells to bring about this response? So we're now looking...

at the off state before epinephrine is released and in this moment the receptor is unbound there's no epinephrine in the system there's a nearby membrane protein that's called a g protein a g protein is not a receptor it's a membrane embedded protein and it can oscillate between two states now it's off it's inactive nearby the g protein is a membrane embedded enzyme not a receptor but an enzyme that's called adenaline. cyclase that is actually the correct pronunciation and it's also in the off state and as a result it's not activating the second messenger what happens when epinephrine enters the system first thing that happens is that epinephrine binds with a G protein coupled receptor. So here's epinephrine, and here it's binding with the receptor. This is a complicated protein, and we've talked about allosteric shifts in relationship to enzymes where where when something binds at an allosteric site, it can then change the active site. Well, the same mechanism is at work here.

Epinephrine's binding over here, and that change kind of ripples through this protein and it induces a change over here. Now, right at this moment, the nearby G protein is still dormant. It's still bound to GDP. GDP is a relative of ADP, and it's the low energy form.

It can oscillate. between this low energy form and a high energy form that we're going to see in a minute and that happens when the G protein becomes activated. What's the effect on the G protein of epinephrine binding with the receptor?

Well the G protein is then able to interact with the receptor. We noted before that the receptor has changed on its cytoplasmic side and that enables the G protein to interact with that part of the receptor and that causes the G protein to discharge GDP that's the low energy form and to bind with GTP that's the high energy form and again notice that this has three phosphates over here just like ATP this only has two phosphates over here like a DP the result is that the G protein now becomes activated so what happens to the G protein once it's bound with GTP it drifts in the membrane it ultimately binds with adenylal cyclase, this membrane-embedded enzyme. That activates adenylal cyclase. And adenylal cyclase's substrate is ATP, and it converts it into a molecule called cyclic AMP, which is the second messenger in these G-protein coupled receptor systems. Note that ATP is triply phosphorylated.

This only has one phosphate, and the AMP stands for adenosine. monosine mono, mono as in one, phosphate. What have we done?

We've taken our initial messenger and we've transduced it, creating the second messenger. So let's review what we've talked about so far. We've talked about reception.

We have the ligand, which is epinephrine. It binds with the G protein coupled receptor. The receptor changes shape on its cytoplasmic side.

It interacts with the G protein, causing it to discharge DDP. which is what it's bound to when it's dormant and bind with GTP which is what it binds with when it's active. The G protein then in turn can activate adenylal cyclase which takes its substrate ATP and converts it into cyclic AMP, the second messenger.

What we're going to look at next is the cellular response. The second messenger, cyclic AMP, is going to activate a chain of relay molecules. These are called kinase. or kinases. And this activation involves one kinase activating the next kinase activating the next.

I've only put three in this chain, but there can be many, many more, and that's called a phosphorylation cascade. How does that phosphorylation cascade work? The kinases are activated by phosphorylation, by gaining a phosphate. And once they're activated, what they do is they activate the next kinase in the chain.

So here Here we have protein kinase one that acts upon protein kinase two by phosphorylating it. So now protein kinase two is active, phosphorylated. What does it do?

It activates protein kinase three by phosphorylating it. I've only shown three, but there can be many more in this chain. And we get this domino-like effect of one kinase activating the next and activating the next. Once we get to adenylal cyclase then each step involves multiple activations. Adenylal cyclase will activate many cyclic AMPs.

Each of these cyclic AMPs will start different phosphorylation chains and the result is signal amplification. We had one epinephrine enter the system but by the end and I couldn't of course depict that here but you'll have the activation of millions of enzymes to bring about a massive cellular response. In the case of liver cells, and the way that they're acted upon by epinephrine, the response is activation of the terminal enzyme, which is glycogen phosphorylase. And what glycogen phosphorylase does is it converts glycogen, again, a polysaccharide.

into glucose, a monosaccharide, that glucose diffuses into the blood, giving you energy for the fight-or-flight response. Are you asking yourself, how am I going to get a 4 or a 5 on the AP bio exam? It's a a good question because it's a hard test but we have a plan for your success go to learn-biology.com sign up for a free trial and complete our interactive tutorials and interactive ap bio exam reviews we guarantee you a four or five on the ap bio exam see you on learn-biology.com topic 4.5 feedback and homeostasis what is homeostasis what are feedback mechanisms and how do they to homeostasis. Homeostasis is the tendency of a living system to maintain its internal conditions at a relatively constant optimal level. Your body temperature, for example, stays around 37 degrees Celsius 98.6 Fahrenheit despite fluctuations in the external temperature.

The changes in your body to maintain that temperature, that's a great example of homeostasis. Feedback is when the output of a system is also an input. So here we have some system, here's the thing that's coming out, and feedback is when it feeds back into the system.

So the output is also an input. And feedback can do two things. One is connected to homeostasis. It can allow organisms to maintain homeostasis as they respond to internal and external changes, just as I told you with temperature. Or it can accelerate internal changes and drive a process towards a conclusion.

This is generally connected with what's called negative feedback, and this is connected with what's called positive feedback. Let's talk about set points. What is a set point? How are set points used in negative feedback? First, a word about the method here.

We're going to talk about this in relationship to your home heating and cooling system. It's much easier to understand this before we look at the biological examples. So a set point is where you set the thermostat. It's the value around which. which a homeostatic process fluctuates.

So above, the set point for the thermostat is 68 degrees Fahrenheit. In negative feedback, the output of the system feeds back to the system in a way that decreases the system's output. So here we have the set point. Here's a measurement of the temperature.

The set point is above the temperature. That'll send a signal to turn on the furnace. That'll generate heat.

Heat feeds back to the system. There's a thermostat over here with a thermometer that will increase the temperature and then when we get to 68 degrees Fahrenheit, the set point, the system will turn off. Negative feedback promotes homeostasis, returning a system to its set point.

How can antagonistic negative feedback loops be paired to promote homeostasis? So, same goal, keep the temperature at 68 degrees. Well, here we have a negative feedback system that responds when conditions are are above the set point. So temperature 70, the set point is 68. What will you do? You'll have a signal that turns on an air conditioner that will put out cool.

It's a real word. And that will feed back to the system. And eventually it'll get the system to turn itself off.

There's been cooling and we've therefore lowered the temperature. But we still have a heating system. And if the temperature goes below the set point, then that's that system would turn on, it would release heat, that would feed back to the system and that would wind up turning the system off.

So we have paired antagonistic systems, one for cooling, one for heating. Now we're gonna look at some biology. Let's talk about how feedback works in blood sugar homeostasis.

It's important to your body to maintain your blood sugar levels, your blood glucose levels. The main hormone that controls that is insulin and it's a negative feedback system. And response. to high blood glucose levels after eating a sugary or a starchy meal, your pancreas will release the hormone insulin, just represented here as a triangle.

In the liver, insulin will bind at a receptor over here, and that will unleash a signaling cascade, and that talks to a glucose transporter. That's a channel that allows for facilitated diffusion. If glucose is in higher concentration outside, then inside the cell, it'll... diffuse into liver cells and the glucose will get converted into glycogen, which is a storage polysaccharide, or it'll get converted into fat.

Blood glucose levels down, homeostasis restored. But as with our home heating and cooling system, insulin is paired with another hormone. So let's explain how insulin and glucagon maintain blood glucose homeostasis.

Our blood glucose has a set point about 90 milligrams per hour. per deciliter. Above the set point, the pancreas will release insulin. Eat a big meal, insulin gets released, and your liver, fat, and muscle cells, which aren't shown, will absorb glucose and store it away as glycogen.

Below the set point, that's when you've gone a little while without eating, what'll happen is that the pancreas will release a second hormone called glucagon, and that will induce the liver to convert its stores of glycogen. into glucose. Glucose goes into the blood, homeostasis is restored. An important AP bio skill is explaining what happens when systems get disrupted.

And here we're going to explain how blood glucose homeostasis breaks down in type 2 diabetes. That's also called adult onset diabetes, but increasingly it's happening in teens and even children due to the obesity epidemic in the United States. We're going to look at normal metabolism first, which we just discussed. Here we see insulin in response to a high blood glucose level is binding with the insulin receptor.

There's a signaling cascade that causes the glucose channel to open. There's glucose absorption into the cells, blood glucose level falls, homeostasis restored. In people with type 2 diabetes, what happens is that the cells become insulin resistant. There's glucose in the blood, there's insulin released from the pancreas, but the binding...

of insulin does not lead to the signaling cascade and because of that the glucose channel remains closed because of that blood glucose level stays high and that damages organs and tissues breakdown of homeostasis leading to type 2 diabetes we just discussed adult onset type 2 diabetes how does that compare with type 1 diabetes type 1 is also known as juvenile diabetes It's an autoimmune disorder, and basically what happens is that cells of your immune system attack the pancreas cells that produce insulin. Therefore, those cells can no longer secrete insulin, and therefore, even in response to a high blood glucose level, insulin is not secreted. That can only be treated by insulin injections.

Type 2 diabetes we've just discussed, also called adult onset, and that involves insulin resistance where the receptor is become. insensitive to the insulin signal. All of the biological feedback loops that we've talked about so far relating to blood sugar have involved negative feedback loops. What about positive feedback loops?

How does positive feedback work? Explain how positive feedback works during childbirth. So in positive feedback, the output of a system feeds back into the system, increasing the system's activity and output. It doesn't involve quieting that leads to homeostasis.

It involves acceleration. It drives a biological process such as childbirth to a conclusion after which the system shuts down. In childbirth the growth of a baby activates uterine stretch receptors. The uterus among other things is a big muscle and that muscle is stretched out.

It sends messages to the brain. The brain releases oxytocin, a hormone. That oxytocin then circulates in the blood when it's picked up by receptors in uterine cells that leads to more contraction. That increased contraction leads to more oxytocin release, and ultimately that continues until the baby is born. Explain how feedback leads to fruit ripening.

If you were to pause the video and take a look at this diagram, I'll bet you that you could figure it out. This is a positive feedback system. Ripening in fruit leads to the release of a hormone that is a gas.

It's called ethylene. Ethylene receptors in nearby fruit pick up the ethylene and that induces additional ripening and more ethylene production. That increased concentration of ethylene accelerates the ripening process in all the fruit, leading to more ethylene. So eventually all the fruit ripens. In fruit shipping, you can prevent that by pumping carbon dioxide into the storage container where the fruit are and that suppresses the ethylene and that's how you can ship fruit longer.

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Topic 4.6, the cell cycle. On a big picture level, what does mitosis do? List three of its key functions in living things. Note for this question that mitosis as it often is, is synonymous with eukaryotic cell division. Mitosis duplicates the chromosomes of a eukaryotic cell, transmitting that cell's entire genome to its daughter cell.

So here you have the parent cell, it's got two chromosomes. Here those chromosomes have been duplicated, now they're being pulled apart, and now you have daughter cells, each with two chromosomes, and each one is going to be an exact clone of its parent cell. parent cell. In a multicellular organism like you and me, mitosis is how an organism grows and repairs itself. Remember that you started life, as all multicellular beings do, as a single cell.

In a unicellular eukaryote, like a paramecium or an amoeba, mitosis is how reproduction occurs. Describe what happens during the cell cycle. The cell cycle, as you can see in this diagram, can be divided into two main phases.

So the outside orange part of the circle, that's interphase. This yellow part over here, that's mitosis or M phase represented by the letter M. During interphase, you can subdivide three basic phases, but the cell doesn't appear to be dividing during interphase. The first is G1, and during G1, the cell increases in size. G1 stands for growth phase one.

During S, which stands for synthesis, you have DNA replication or chromosome duplication. And during G2, growth phase 2, you have the growth of the structures that are required for cell division. During M phase, you have mitosis, separation of the chromosomes followed by cytokinesis. So at the end, you have two donor cells that are clones of the parent cell.

Describe the phases of mitosis. We begin with interphase during which the cell grows and replicates its DNA. During that time, it doesn't look as if it's dividing, but DNA replication, for example, has occurred. During prophase, chromosomes, which are spread out as what's called chromatin during interphase, they condense into these X-like structures. The nuclear membrane disintegrates, and a spindle apparatus, which is these fibers over here, you can see the entire apparatus in the next phase start to grow from each centrosome.

During metaphase, the spindle fibers grab onto the chromosomes and they pull and push them to the cell equator. If you can sort of imagine a line running down from top to bottom, that would be the cell equator. I talked about this X-like formation that the chromosomes are in.

That's because each chromosome is doubled and consists of two clones called sister chromatids. During anaphase, the spindle pulls the sister chromatids apart and starts dragging them. to the opposite ends of the cell.

At the same time, there are what are called non-kinetochore microtubules. A kinetochore is like a handle on the chromosomes that these spindle fibers use to pull the chromosomes apart. But there are other fibers that basically push on one another, and that causes the cell to elongate.

During telophase, a new nuclear membrane starts to grow around each set of chromosomes. The chromosomes spread out into their interphase formation. so you can't really see them anymore. And a nucleolus reappears in each cell.

It disappeared during interphase. The nucleolus makes ribosomes, and ribosome production shuts down during most of mitosis. Finally, during cytokinesis, the cell splits apart into two daughter cells.

I have a great song about mitosis. Mitosis, chromosomal ride, in a chromatic anaphylophase divide. You carry out scope from one cell to two.

Mitosis, how cells renew. and I'll put the link below. Explain the importance of the G0 phase of the cell cycle.

Basic idea here is that not all cells go through the entire cell cycle. So if you have highly specialized cells, like a nerve cell or a muscle cell, they'll leave the cell cycle and they'll enter into G0 after which they won't divide. Certain stimuli however can induce cells in G0 to re-enter the cell cycle. Topic 4.7, regulation of the cell cycle.

Describe the role that checkpoints play in regulating the cell cycle. Cell cycle checkpoints are moments when the cell checks its internal conditions and decides whether to progress to the next phase of the cell cycle. If If certain molecules are in the right concentration, then the cell continues through the cell cycle.

And if not, the cell moves into G0 or might initiate what's called apoptosis. We'll explain that in a moment, which is called programmed cell death. The primary checkpoints to know about for AP Bio are the G1 checkpoint over here, the G2 checkpoint, and the M checkpoint. What is apoptosis? I've talked about that several times.

I know that. the second p is silent apoptosis is programmed cell death it's part of a signaling cascade that involves the mitochondria and the nucleus it's highly regulated which is very different from cell death that results from traumatic cell injury cells are broken down into cytoplasmic fragments that are called blebs you can see some of those over here and over here and blebs are consumed by cells of the immune system preventing cell cellular debris and enzymes from damaging nearby cells. What are cyclins and cyclin-dependent kinases?

Cyclins and cyclin-dependent kinases are important internal regulators of the cell cycle. The cell cycle is regulated by outside signals, but also by internal conditions. Cyclins are molecules whose concentration rises and falls throughout the cell cycle.

So like for example, you can see that cyclin E rises. right before the S phase. Cyclin A rises right before G2. The cell has mechanisms to read the level of these cyclin concentrations. Kinases, which we discussed previously in the context of cell communication, those are molecules that activate other molecules often by phosphorylating them.

They're not shown. And cyclin-dependent kinases, or CDKs, are kinases that respond to rising and falling levels of cyclin levels. Now we're going to put that all together and see what some of the mechanisms are that regulate cell division.

Explain how the interactions between cyclins and cyclin-dependent kinases control the cell cycle. So CDKs, here they are over here, are present at a constant level throughout the cell cycle. By contrast, the level of cyclins that we saw in the previous slide rise and fall.

When cyclin levels are high, the cyclins... bind with CDKs to form a complex called maturation promoting factor, but a good way to remember that is just think of it as mitosis promoting factor, because once you have MPF, that allows the cell to pass through the G2 checkpoint and actually divide. During M phase, however, the cyclin is broken down, and that allows the process to repeat in each donor cell when it grows to the appropriate size and gets ready. for cell division.

We talked about the cell cycle, now let's talk about dysregulation of the cell cycle. What's the connection between cell division and cancer? What are the two types of genetic mutations that are connected to cancer? Cancer is a disease of unregulated cell division.

As opposed to cells staying in place doing what they're supposed to do, they become rogue players pursuing their own destiny at the cost of the organism. Mutations in genes that are called called proto-oncogenes increase cell division by creating too many growth factors. Growth factors are things that stimulate cell division within a cell itself or within other cells. And there are other kinds of genes that are called tumor suppressor genes.

And what they do is they remove cell division inhibitors, the kind of checkpoints that we've seen in previous slides. So in normal cells, you have the breaks. Those are tumor suppressors.

And you have the accelerator. Those are growth factors, but they act at appropriate times. When cells become cancerous, it can be for one of two or actually both reasons. You can have mutated tumor suppressors. that can't prevent cell division, even when cell division shouldn't be happening.

And you have growth factors that promote cell division at unneeded moments. Describe how a mutation in the Ras proto-oncogene can induce a non-cancerous cell to become cancerous. What we're gonna do now is really cool because we're gonna connect what we've learned about the cell cycle and its control to what we learned about previously relating to cell communication. So, Ross is a G protein over here and as a proto-oncogene it only becomes active when an outside growth signal binds with Ross's coupled receptors. So here we have binding that activates Ross, it picks up GTP that sets off a phosphorylation cascade and that leads to cell division.

So this is in a healthy normal system. Ross only gets activated when there's a ligand. When ROS becomes cancerous, when it mutates from a proto-oncogene to an oncogene, then it becomes constitutively active.

And constitutively means it's part of its nature to be active. Normal ROS is only active, it only binds GTP when the receptor binds a ligand. But this ROS, which is an oncogene, is constitutively active.

It's binding GTP even in the absence of a growth signal. And because it's always active, the growth factor over here is overproduced, and that results in too much cell division. This is connected with about 30% of human cancers.

Describe how a mutation in a tumor suppressor gene such as p53 can contribute to the development of cancer. P53 is a tumor suppressor gene. When the cells experience DNA damage, a signaling cascade, activates p53. So here we have DNA damage, it's detected, there's a signaling cascade, and now p53 is activated.

If the damage can be repaired, then what p53 will do is it'll halt the cell cycle while DNA repair enzymes fix the damage. So we're going to fix up the DNA, that's what's happening over here. If the damage is too great, then p53 will initiate a whole signaling cascade that will cause the cell to initiate apoptosis.

So either we have repaired DNA that occurs while the cell cycle is halted or the cell will self-destruct. Cancer has been prevented. If mutations lead p53 to become non-functional, then the cell will continue to divide even with damaged DNA. So here we have DNA damage. It's been detected.

but p53 can't do anything about it therefore there's no stop signal the cell will continue to divide and that will increase the chance of the cell acquiring further mutations that can lead it to become cancerous again dysregulation of a signaling cascade dysregulation of a cell cycle repair mechanism leading to cancer here are your next moves on your journey to ap biosuccess number one Go to learn-biology.com, sign up for a free trial of our AP Bio curriculum. We guarantee you're four or five. And then watch this next video.

Transcript for:AP Biology Unit 4 Exam Review Guide

Transcript for:
AP Biology Unit 4 Exam Review Guide