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Welcome to AP Bio unit 7 evolution. This is the climax of an AP biology course and it can also be really intimidating stuff. You're looking at hundreds of millions, billions of years of biological evolution. How do we explain that change through time? The first topic is selection, natural selection, artificial selection, sexual selection. Then we'll delve into population genetics and the Hardy Weinberg equilibrium. We'll spend a lot of time looking at the evidence
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for evolution. That'll lead us to looking at how species diverge into multiple descendant species. That's the idea of speciation. We'll look at variation in populations. We'll look at life's branching pattern and history, which is the topic of phylogeny. And then we'll end by looking at the origin of life. I'm Glenn Wilenfeld, also known as Mr. W. And I love teaching. B I O L O G Y. To help you study, I've put together a checklist that you can download at apbiosuccess.com/checklist.
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Natural, artificial, and sexual selection. In terms of understanding the process of evolution, the most important idea to understand is natural selection, developed by Charles Darwin in the 1800s. Darwin himself built the idea of natural selection upon the foundation of artificial selection. So, that's where we're going to start. Artificial selection is also known as selective breeding. And in this process, breeders envision
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a desired trait in an animal or a plant. For many generations, the breeders select organisms with that trait. And the process over time, over many generations, creates a carefully guarded gene pool with individuals that only have genes for the desired trait. Here are two examples. The plants that are in the Brassica oleracea family include cauliflower, broccoli, Brussels sprouts, etc. They're all the same species. The ancestral plant Brassica oleracea has been bred
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for specific traits, for flower clusters, in terms of cauliflower, for flower buds, in terms of broccoli, for lateral buds, in terms of Brussels sprouts, for kale, in terms of leaves. But all of these are varieties of the same species that have been bred for specific traits. The same is also true of dogs. Dogs and wolves are all members of the same species. Canis lupus and all the breeds varieties of dogs. The German shepherds and the Schnauzers and the dachshunds.
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Those are all varieties that have been bred for specific human purposes, for protection, for hunting, or for just looking cute and being really cuddly. So, how does natural selection work? In any population, there's variation. The kind that matters is inherited variation that's in the genes, and that comes about through recombination and mutation. In any population, the reproduction rate, the number of individuals who were born exceeds the survival rate. And that's
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even true of slow-breeding populations. Sometimes that's summarized by the phrase, "Many are born, but few survive." The survivors have a beneficial trait that gave them some type of advantage. As the generations proceed, mutation continues to create new variants. And if you repeat steps one through four, you wind up with adaptation. Adaptations can include things like the incredible structure of the wing of a bat or the incredible behavioral adaptation, which is sonar, which is
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of course combined with structures like the ears of a bat, which can hear high frequency sounds. They can be camouflage mutations like this satanic leaf gecko or they can be on a molecular level like the way that enzymes fit with substrates. You've learned a lot of biology and whenever you see things and you find yourself thinking, how could that work? How could that be so perfectly put together? It was put together by natural selection. In addition to artificial
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selection and natural selection, a third type of selection to know about is sexual selection. Sexual selection is selection for traits that directly increase reproductive success. They create an evolutionary dynamic that results in sexual dimorphism where there are different phenotypes in males and females. One type to know about is called intersexual selection. And that's where members of one sex, typically the females, choose mates of the other sex
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that are typically males. So here's a photograph that I took relatively near to my home. This is a female turkey. There's a bunch of male turkeys who are displaying to her and they're essentially saying through their movements and through their extension of their tail feathers, I'm really attractive. You should mate with me. And that means that there's been selection for these tail feathers and for features like these wattles and for the male's behavior. Peacocks are a bird
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species where that's been carried to extraordinary lengths and that typically leads to colorful and highly adorned males and choosy females. The other kind of selection is called intrasexual selection. And that's where competition between males for control of a harem of females or control of a breeding territory leads to a dynamic where the males are aggressive and often really big and strong. And that's what we see over here with these elephant seals that live off the coast
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of Northern California. And they're about twice the size of females. They're huge, aggressive, testosterone animals. Selection can change the distribution of phenotypes in a population in a variety of ways. In any population, most characteristics can be represented by a bell curve of continuous variation. If you took all the students in your school and you organize them by height, most of the people are average height. There are a few people who are short
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and a few people who are tall. That's a bell curve distribution. Directional selection, which is shown over here, selects against one of these extremes. In other words, here's the original population. You're selecting against this extreme over here. And so, you're pushing the population in this direction. In stabilizing selection, you are selecting against the two extremes. An example of stabilizing selection is birth weight in babies. Babies that are too
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small have lower survival. Babies that are too big have lower survival. The babies who survive most are the ones who are of average size. The third type is called disruptive selection. If you can imagine a scenario where the average phenotype is maladaptive, then there would be selection for the two extremes. It would kind of split the population into two. An important type of directional selection to know about is adaptive melanism. Adaptive melanism is the darkening of
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the body within a population in response to the darkening of the environment. It occurs within a population as its gene pool evolves in response to natural selection. So it's not like getting a tan which happens in an individual. This is something that happens over evolutionary time as genes for light coloration are selected against and genes for darker coloration are selected for. The selective pressure that results in adaptive melanism is typically predation.
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What's shown here in this example is the rock pocket mouse which lives in the southwest of the United States. And what's been documented on a genetic level is that populations of these mice that live on a dark colored substrate have evolved a mutation that results in more melanin production. And that mutation spreads throughout the population and results in subpopulations that have the dark coloration. We've been talking about various types of selection. Natural selection
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is often summarized as survival of the fittest. What does it mean to be fit? How is evolutionary fitness measured? Evolutionary fitness is not about strength or speed. It's the number of offspring and offspring of offspring that survive to reproduce. And the reason why I have this montage of penguin life is just to indicate that it is something that emerges at every level of the life cycle. When the penguins are feeding, when they're doing their march inland,
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when they're breeding, when they're juveniles huddling together, there's fitness at every single stage. And fitness throughout the life cycle is what enables genes to be passed on to the next generation. To end this discussion of all types of selection, we're going to look at this question. Explain how the peppered moth demonstrates an evolutionary change in response to environmental change. The key point about the peppered moth is that it provides science with a directly observed
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example of directional selection and adaptive melanism in response to an observed change in the environment. The peppered moth comes in two forms. There's a peppered form, mostly light colored, and a dark form. And before the industrial revolution, the industrial revolution began with the invention of the steam engine, the burning of coal. The predominant phenotype was peppered was this one over here. So in any population of moths, almost all of them were peppered. There'd
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be a few dark moths. Why is this? Because that was a form of adaptive coloration. The moths were camouflaged as they rested on light colored tree trunks which were often covered by these whitish colored lichens. That's the situation before the industrial revolution. With the industrial revolution, soot from factories was put into the air. It landed on the trees. It killed the lichens
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and darkened the tree trunks. And what that did is that it created a selective advantage for the dark colored moths. If you were to do a census of the moths at the beginning of industrial revolution, most of them were white. Only a few were black. But as the industrial revolution proceeded, the mean phenotype shifted from light to dark until in the depths of the industrial revolution, the majority of the moths were dark colored. The interesting thing is that this process was
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also historically reversed. About 1960, soot from pollution declined with the development of laws like the Clean Air Act that happened around the world. The lichens returned. The trunks became lighter. The mean phenotype of the peppered moth shifted from dark colored to light colored. I have a song about the peppered moth. And there's also fascinating stuff related to the history of this because it was embroiled in some controversy. But the work of Michael Majerus
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which was done in the early 2000s which replicated some work done by B. D. Kettlewell which was done in the late 1800s or early 1900s. established this as a clearly observed case of adaptive melanism phenotypic shift in response to an environmental change. Your success in AP biology starts here. Are you struggling with AP bio? With learn-biology.com, students get the skills and confidence to be a top student and earn fours and fives on the AP bio exam guaranteed. Go to
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learn-biology.com to find out how you can master your biology course and crush the AP bio exam. Population genetics and Hardy Weinberg. What is population genetics? Population genetics is a study of how genes are distributed in populations and how they change over time. Key thing that we measure in population genetics is allele frequency. In this population over here, we have 20 individuals and we're tracking the frequency of the allele big A and little A. And we can see that
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the frequency of little A is 0.5. It makes up 50% of the alleles in this gene pool. What is a gene pool? It is simply all of the alleles of all of the genes in a population. And in that context, evolution means a change in the genetic makeup of a population over time. It's the change of allele frequencies within a gene pool. Before we get more into the details of population genetics, I want to
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address the biggest misconception I've seen among my students related to population genetics. That's the wrong idea. That's why it's crossed out that the dominant allele has to be more common than the recessive allele. These are different dimensions of biological analysis. And allele frequency, whether an allele is common or rare, has nothing to do with dominance or recessiveness. It's based
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on the advantage or harm an allele confers to its associated phenotype or random historical factors. And here's an example. The allele for the condition called achondroplasia is exceedingly rare, but it's a dominant allele. Population genetics is one of the more mathematical parts of the AP curriculum, and it's built around two equations. P + Q = 1 and P ^2 + 2 PQ + Q ^2 = 1. In this system, P represents the frequency of the dominant allele and Q represents the
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frequency of the recessive allele. If you load P + Q into a Punnett square, the whole thing makes a lot more sense. P + Q= 1 means that for a gene with two alleles, the frequency of the dominant allele and the frequency of the recessive allele equals all the alleles. P + Q = 1. P ^2 + 2 PQ + Q ^2 = 1. What does that mean? Well, first of all, here's P and here's P. If you do the Punnett square kind of thing, this would be P^2. The frequency of homozygous dominance,
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P^2 plus the frequency of heterozygote, PQ + PQ= 2PQ, plus the frequency of recessive individuals, Q squared, is all the individuals in a population. And you can see that right here. Here's how you might see this in a sample problem. You've identified, you've been told that 49% of the mice in a population have the recessive trait of white fur. Figure out the frequency of P, Q, P ^2, 2PQ, and Q ^2. So here's our original setup. What we're going to do is Q^2 is this
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value over here. So we're just going to put 0.49 over here. From there, what we're going to do is we're going to work to figure out that the square root of 0.49 is 0.7. Then we know that this plus this equals 1. So therefore this the value p has to be 0.3. Then we know that 2 pq has to be 0.42. Why? 0.3 * 0.7 is 0.21 * 2 is 0.42 and p ^2 is 0.09. 0.3 * 0.3 is 0.09. if you set up Punnett square cross multiplication tables you'll get this right every time the Hardy–Weinberg
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principle is that the frequencies of alleles in gene pools will stay constant unless one of the more following conditions is not met this Hardy Weinberg population is a fictional population that's used to understand what causes evolutionary change in real populations. The first is that the population is infinitely large. There are no harmful or beneficial alleles. There's random mating. There's no immigration or emigration. And there's no net mutation of one allele to another.
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If any of these five conditions is violated, then allele frequencies can change. And these are the factors that can cause evolution. What are these factors? Small populations leading to a phenomenon called genetic drift. Natural selection where certain alleles are beneficial and others are harmful. Sexual selection which is the opposite of random mating. Gene flow where genes move into a
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population or out of a population. And directional mutation where one allele has a tendency to mutate into another allele. So what's genetic drift? And we'll also look at one variant of genetic drift called a population bottleneck. Genetic drift is a random change in allele frequencies in a population's gene pool, usually associated with small population size. A population bottleneck can cause genetic drift. A biotic living or abiotic non-living factor wipes out a large percentage
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of the individuals in a population leaving only a few survivors. The survivor's alleles might not be representative of the allele frequencies in the former larger population and some alleles might disappear completely. The reason why I have a picture of a cheetah here is that cheetahs are extraordinarily genetically uniform. It's as if all cheetahs are practically identical twins or at least very close siblings. Based on genetic analysis, it looks like the cheetahs underwent
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some enormous population bottleneck. maybe a viral infection or something like that that wiped out almost all of the cheetahs down to only a few individuals. They repopulated from those few individuals, but as a result, many alleles were lost and they're highly genetically uniform. Note that in a population bottleneck, the survivors didn't have any advantage. It's not natural selection. They were just lucky. Another form of genetic drift is the founder effect. And
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this is where a small number of individuals from a large population founds a new population. But because of insufficient sampling because it's only a few individuals who leave the larger population, the allele frequencies of the gene pool of the founders who found the new population might be different from those in their parent population. In this graphic over here, here's the original
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population and the squares and circles represent different alleles. The founders go off to colonize three islands. In this situation over here, the blue allele is completely lost and now the red allele is at 100%. Here there's a representation of the diversity of the former population. And in this case, the red allele is lost and the frequency of the blue allele is now at 100%. What is gene flow and what's its effect on evolving gene pools? Gene flow is the movement of
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alleles from one population to another. And that can involve the movement of individuals like we see here. This beetle is moving from population 2 to population one. But it can also involve the movement of gametes. And that's easier to imagine in the case of plants where pollen is flying from one field to another. What's the effect of gene flow? It can change allele frequencies especially in the recipient population and it can diminish differences between adjacent populations.
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Mutation is one of the conditions that violates the Hardy Weinberg equilibrium. So what's its importance to evolution? Mutation is the ultimate source of genetic variation within and between populations. And if it's directional, if allele big A tends to mutate to little A, then it can change allele frequencies within a population. Here's a population genetics illustrative example. Sickle cell disease is caused by a recessive allele in the gene for hemoglobin.
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It can significantly decrease the quality of life and lifespan. Yet the allele is in high frequency in certain populations. Explain sickle cell disease is caused by a point mutation in the gene for hemoglobin. It results in the substitution of valine a non-polar amino acid for glutamic acid an acidic amino acid. It occurs only in children who are recessive for the allele. But heterozygotes
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can experience a small amount of sickling, not enough to generate pain crises and tissue damage under most circumstances. The red blood cells in heterozygotes despite the fact that they don't normally sickle are hostile environments for the Plasmodium parasite that causes malaria. This is a parasite that's carried by mosquitoes and then lives inside red blood cells. So what we have is
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a phenomenon that's called heterozygote advantage where big S big S homozygous dominant is selected against. Why? Because of malaria. Big S little S heterozygosity is selected for. Why? because it doesn't have the symptoms of sickle cell anemia but it provides protection against the malaria parasite and small s small s is selected against because you have sickle cell disease. What this map shows is the high correlation between the frequency of the little s allele and the
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intensity of malaria in various parts of Africa. And this same model, heterozygote advantage, might apply to genetic diseases like cystic fibrosis and Tay-Sachs. I'm Mr. W from learn-biology.com where we believe that interaction and feedback is what leads to deep substantial learning. We're so sure of that that we provide a money back guarantee that comes with your subscription. Evidence of
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evolution. There is abundant evidence to support the theory of evolution for AP bio. The most important type of evidence to know about is the idea of homologous traits. Homologous features. Homologous traits are traits that share a common underlying structure and a common embryological origin. They show descent with modification from a common ancestor. Here's the forelimb of a human, dog, bird, and whale. The bones that make up their forelimbs have been given the same name
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by anatomists who recognized that they were the same bones. You can also see that they develop from the same piece of tissue embryologically. It's because these structures evolved from a common ancestry who had these structures and then natural selection evolution led these structures to evolve differently in different lineages. Homologous features result from an evolutionary pattern that's called adaptive radiation. Adaptive radiation occurs when one
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parent species produces several descendants, each of which has unique adaptations and fills a different ecological niche. These are some of the finches that live on the Galápagos Islands. They are all the descendants of an ancestral finch that was blown over there from Ecuador, a small population of finches, and that evolved in different directions. What's the connection? These are descendants of the same species and their beaks are actually homologous features.
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They descended from a common ancestor. They became modified in each of the descendant species in different ways. A vestigial structure is a special kind of homology that provides further evidence for evolution. A vestigial structure has no apparent function but it was inherited from an ancestor from whom that structure had a function. For example, whales have no hind limbs, but they have a pelvis over here onto which to attach those limbs. Why do they have that? Their
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ancestors possessed hind limbs, which were lost as whales adapted to their aquatic lifestyle. We have a coccyx, a tailbone. This is homologous to the tails of cats and dogs and other vertebrates, other mammals. We lost it in the course of our primate evolution into one of the great apes. What can be confusing when you're looking at common features to draw evolutionary connections are the
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difference between homology and analogy. Analogous features have a similar function, but when you look deeply, there's a different underlying structure. They arise through a different kind of evolution, not adaptive radiation, but convergent evolution. And an example is shown here. We have sharks. We have Ichthyosaurs, an extinct kind of reptile, and we have dolphins. They all have a hydrodynamic form, and that's a convergent solution to the challenge of swimming. Here's a
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tricky question. Are the wings of birds and bats analogous or homologous? Think about the answer, then see mine. The wings of birds and bats are a convergent solution to the challenge of flying. They did not evolve from a common ancestor. Bats evolved from some ancestral mammal that was probably like a rodent. And birds are dinosaurs and they evolve from small land living dinosaurs.
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The function of the bird wing, the function of the bat wing is similar. But the underlying structure, the organization of the bones is different. The wings are an analogous structure. But if you look at this question a little bit differently, you get a different answer. The forelimbs of birds and bats are homologous. They're are the same bones inherited from a common ancestor. So another example of why on the AP bio exam or in your AP bio course, you need to carefully read
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the prompt and think before you answer. What are molecular homologies? How do they serve as evidence for evolution? Molecular homologies are homologous features but at the molecular level. They're molecules that by their structure and monomer sequence indicate common ancestry. All vertebrates, for example, have hemoglobin that has the same structure two alpha chains two beta chains. Many of the amino acids are the same. But as you might expect, the closer an animal is to
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us morphologically, the closer its hemoglobin is to us in terms of amino acid sequence. So there's only one difference in amino acid sequence between us and gorillas. Between rhesus monkeys and humans, there are eight differences. Mice, which are also mammals but not primates, there are 27 differences. Chickens, which are yet more distantly related to us, have 45 differences. And frogs, which are the most distantly related, have the greatest amount of difference, 62 differences.
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Pseudogenes are yet another category of evidence for evolution and they're really extraordinary. A pseudogene is a nonfunctional gene that's a variant of a functional gene in a related species. An example is the GULO pseudogene that humans have as well as most of our primate cousins. Here's the GULO pseudogene. It has a series of mutations that keep it from working. Perhaps the mutation is in a broken promoter. Or perhaps the mutation is in the structural genes, but rodents have a
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functional version of this gene. It enables them to produce the enzymes to synthesize vitamin C, but primates can't do it. Why do we have the remnants of this gene? It's a molecular vestigial feature. These pseudogenes only exist because of descent with modification. We and rodents share a common ancestor over here. That common ancestor had the GULO gene and it was able to produce the enzymes to synthesize vitamin C. We primates lost the ability to do that. A mutation emerged,
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broke the gene, but because we lived in a fruit environment, that mutation wasn't selected against. What's really fascinating is that we're not the only mammals that have that pseudogene. It's also found in guinea pigs and it's also found in bats. But if you look at the sequence of those pseudogenes, they have different mutations from our pseudogenes. So this pseudogene, this pseudogene, and our pseudogene, those are all convergent features. They're analogous, not
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homologous. Biology. So amazing. Homologies can take us all the way back to the origin of life. There are a couple of features that show that all living things are related. What are they? DNA used as a genetic material. ATP used for energy coupling, the same genetic code that's universally used, ribosomes used for protein synthesis, shared metabolic pathway like glycolysis, the KREBS cycle, the electron transport chain, and ATP synthesis through chemiosmosis. This shows
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that all living things are cousins. We all share a common ancestor going back to the origin of life. The homologies that we just discussed go back 3.8 billion years or so to the origin of life. There are also more recent ones still ancient that go back 1.8 billion years that indicate that all eukaryotes are cousins. These include the presence of a nucleus, mitochondria or organelles that are derived from mitochondria, the endomembrane system, genes that possess introns, linear
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chromosomes as opposed to the circular chromosomes of prokaryotes and sexual reproduction involving gamete production and fusion of gametes to form a diploid zygote. These are features shared by all eukaryotes. They indicate common ancestry. We're cousins to all the eukaryotes. We're cousins to all life, but we're closer cousins to those in our domain. Eukarya. Describe how embryological development provides evidence for evolution. Early embryos of vertebrates look similar.
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Here's a fish, a reptile, a bird, and a human. During development, the embryo differentiates and that leads to the adoption of the body form of the adults of the lineage. So bird and human embryos quite similar, but we all know what adult birds look like and we all know what adult humans look like. The similarity of the embryonic form indicates common ancestry. There was a common vertebrate ancestor that gave rise to the lineage of fish, reptiles, birds, and humans. Descent with
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modification leads to the elaboration of form in different lineage. The different body forms of fish, reptiles, birds, and humans. But the embryonic similarity along with fossil evidence shows that all of these organisms are descendants of a common ancestor. An additional line of evidence for evolution related to embryos is as follows. Embryos often show vestigial features such as the tail in humans, the pharyngeal gill slit in humans that indicate descent
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with modification from a common ancestor. Diverse species share common genes for animal development. Describe how this provides evidence for evolution. This is a mind-blowing example of homology. In animals separated by hundreds of million years of evolution, shared genes control certain developmental processes. Here's an example. There's a gene that's called Eyeless. That's a master switch that turns on eye development in arthropods and vertebrates. The genes can be
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transplanted leading to successful development. What do I mean by that? Here's a mutated version of Drosophila that doesn't develop an eye. It has a mutant version of the Eyeless gene. You can find mice that have similar mutations that also don't develop eyes. But if you can take the gene from an eye developing Drosophila and implanted it into the eyeless form, it'll develop eyes. But the amazing thing is that if you take the gene from an eye developing Drosophila and put
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it into an eyeless version of a mouse, that mouse will develop an eye. In other words, this doesn't control the eye. The eyes are quite different, but it basically says build an eye. In a fruit fly, it'll build a compound eye. That's common to insects. And in a mammal, it'll build the kind of eye that we have. But there's a master switch that's common to all animals that have eyes that
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control eye development. Another example of that is homeotic genes. These are genes that basically say that you should have a head up here and you should have a tail down there and you should have these appendages over here. And these are common across all animals as diverse as arthropods and vertebrates. And these shared genes again are homologies and they indicate that all animals shared a common ancestor that goes back to the origin of the animal clade about 600 million years
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ago. What is biogeography? How does biogeography provide evidence for evolution? Biogeography is the study of the geographic distribution of species and varieties. If you enjoy looking at birds, as I do, you know that there are certain species that are found on the west coast of North America and there are others that are found on the east coast. That in and of itself is biogeography. The pattern of distribution on the surface of the earth fits the idea that populations first
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evolve in one area then spread to adjacent areas where subsequent evolution occurs. In other words, the pattern of evolution is not only seen through time, it's also seen through space. And a great example of biogeography is the fact that the marsupial mammals are mostly but not completely limited to Australia. Why? Because Australia is a kind of isolated island continent, the only placental mammals that were ever able to get to Australia were the bats, which could fly
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there and a few rodents that were able to reach Australia on floating vegetation mats. But other larger land non-flying placental mammals couldn't get to Australia and hence it's the marsupials that are the predominant mammals in Australia. A fascinating thing connected with the evolution of marsupials is parallel evolution where because placental mammals never made it to Australia, all
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of the niches that are filled by placental mammals in North America and Eurasia and Africa are filled by marsupials and those similarities are all convergent. So the marsupial mole and the eastern mole convergent similarities based on a common niche. They're both digging in the soil. The sugar glider and the flying squirrel and even top predators, the now extinct Tasmanian wolf and the
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wolf that we find in North America and Eurasia. Biogeography, another entire line of evidence for evolution. As we've seen, you can find evidence for evolution in the structure of animals, in their genes, in their distribution over the face of the earth. But you can also find evidence for evolution in time. That's what fossils are all about. What are fossils? How are they evidence for evolution? Fossils are petrified remains of living things. Evolution is change over time, and
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fossils demonstrate this change. As you go back in time, you find different arrays of living things. Through transitional forms, fossils show descent with modification in a variety of lineages. Now, this example over here is an artistic rendition, but it provides the point, which is that as you go back in time, you don't find modern whales. You find the ancestors of whales who have features
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that indicate that whales evolved from animals that once were mammals that lived on land that over time adapted to an aquatic lifestyle. What is relative dating of fossils? How does it work? It's based on the idea of superposition. And the idea is that in rocks that are sedimentary that are laid down layer by layer, the younger material is on top of the older layer. So this would be younger over here and this would be older down there. The deeper layers are older than the
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fossils in layers closer to the surface. That's superposition. But because the earth is complex and because there are earthquakes and volcanic eruptions, there's faulting, uplift and inversions that can complicate this analysis. But based on the position of fossils within sedimentary strata, you can determine which fossils are older than others. In addition to relative dating, determining which fossil is older than others based on their position in sedimentary strata,
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there's also absolute dating. Describe how absolute dating of fossils works. It's based on the decay of radioactive isotopes that are in fossilized remains or nearby volcanic strata that are interspersed with sedimentary strata. The key idea is the idea of half-life. That's the time it takes for half of a sample of radioactive isotopes to decay from one element to another. So an example, carbon 14 decays to nitrogen 14. Carbon 14 is radioactive unstable. It's decays
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to nitrogen 14. The half-life is 5,730 years. If a sample has 50% carbon 14 and 50% nitrogen 14, then for example, if this was a piece of bone, then that bone would be 5,730 years old, it's one half-life. If one-fourth of the carbon 14 is left, then it would be two half-lives, 11,460 years. Other isotopes have longer half-lives. You can find carbon 14 directly in organic remains. But you can also find, as I said before, radioactive elements that are in volcanic strata, and you can
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use that to date older fossils. So that's how we know how long ago the dinosaurs became extinct, when the first vertebrates emerged, when the first fish emerged, so on and so forth. That's absolute dating of fossils. Evolution can be observed in structures that we see in modern organisms, but there's plenty of evidence that evolution continues to this day. A great example of that is shown in this slide. How is evolution of resistance to DDT and mosquitoes evidence
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of continuing evolution? Let's talk about what's happening in this slide. Here's a mosquito. This is showing the percent of mortality of mosquitoes to a 4% solution of DDT exposed to them for 1 hour. DDT is a pesticide kills mosquitoes. Why do we want to kill mosquitoes? Mosquitoes can spread a parasite that causes the bloodborne disease malaria. And malaria is a devastating disease that causes illness in hundreds of millions of people around the world. What happens is that
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when you spray the pesticide, at first it's very effective and it kills most of the mosquitoes, but never all of them. There's always some mosquitoes that have some inborn resistance that survive the initial use of DDT. Those mosquitoes pass on their genes for resistance. Over time, within a matter of months, you have only about 50% of the mosquitoes are killed. Why? Because mosquitoes
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have a very short generation time. So this process is occurring quite rapidly and then after about 16-18 months very few of the mosquitoes are being killed. This is observed genetic change. There's some gene that's producing some protein and that gene is increasing in frequency throughout the population caused by human selection for DDT resistant mosquitoes. This is not the only example of the rise of resistance. There are parallel instances of evolution of resistance that
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have been observed in the evolution of antibiotic resistance in bacteria, resistance to herbicides in weeds, resistance to chemotherapy drugs by cancer cells. It's a phenomenally important example of evolution that we can observe in this day. I want to acknowledge how difficult and complex some of these concepts can be and I want to encourage you to go to learn-biology.com and with a free trial you can do the tutorials and you can use our unit reviews and it's going to really
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help you to get on top of this material setting you up for success on your unit test or the AP bio exam. What is the biological species concept and what are some of its limitations? The biological species concept defines a species as a group of organisms that can naturally interbreed to produce viable meaning healthy, fertile, meaning able to reproduce offspring and which is reproductively isolated from other such groups. Here is an example of one species. There are different
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breeds of dogs, but the dogs don't care. left to their own devices, they'll interbreed and they'll produce viable, fertile offspring. These two species of ducks, by contrast, don't interbreed or at least they interbreed to such a small degree that their gene pools are separate. The concept is not perfect and it falters in a couple of cases. The first is in the case of closely related species which can often hybridize. They can often interbreed but not so much.
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So the gene pools maintain relative separateness, extinct or asexual species, how could you tell if they could produce fertile or viable offspring, and prokaryotic species. What are reproductive isolating mechanisms? Compare and contrast pre and post zygotic forms of isolation. Reproductive isolating mechanisms are processes, behaviors, or other traits that keep the gene pools of closely
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related species separate. Mallards, pinttails, they're both ducks. How do they maintain separate gene pools? There are two kinds of barriers. The first are prezygotic isolating mechanisms and they prevent breeding altogether. They prevent the formation of a zygote. Postzygotic barriers exist between species that are close enough to mate and form a zygote. But formation of a zygote doesn't
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ultimately lead to the production of successful individuals, viable individuals who can survive and produce offspring themselves. Let's look at prezygotic isolating mechanisms. The first kind is behavioral. Different mating rituals or courtship behaviors would keep a female and a male from accepting one another as members of the same species and mating. Temporal means that they would breed during different times of the day or different seasons. One species mates
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in the winter, another mates in the summer, they're not going to interbreed. Mechanical structural barriers that prevent sperm or pollen from reaching an egg. If the flower structure is very different, then a pollinator wouldn't be able to bring pollen from one flower to another flower. Habitat. One species lives in the forest, another lives in a meadow. One species lives in the uplands, another lives in the lowlands. They won't meet each other in order to breed. And finally,
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gametic. The egg won't allow fertilization because there's some molecular mismatch that would keep the sperm from being able to bind with the egg and induce the kind of changes that lead to fertilization. List and describe three postzygotic isolating mechanisms. Postzygotic barriers can exist between species that are close enough to mate and form a zygote, but nevertheless, their gene pools remain separate. These can include hybrid inviability. The hybrid
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organisms don't develop. There might be hybrid sterility. The hybrid offspring are healthy, but they can't reproduce. That's what's going on between horses and donkeys, which can interbreed to produce mules, but the mules themselves are sterile. Finally, there's hybrid breakdown. The hybrids are healthy and can reproduce, but the next generation, the F2s are inviable or infertile. Contrast allopatric and sympatric modes of speciation. Allopatric speciation involves a
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geographic barrier. It's what's shown over here in number one. Sympatric speciation occurs without a geographical barrier as shown over here in number two. In allopatric speciation, geographical isolation leads to genetic differentiation which leads to reproductive isolation. In stage one, a species is spread out over a geographical range. There's gene flow between any subpopulations. In
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stage two, some kind of geographic barrier like this shown at B arises and it splits the species apart. So there's no longer gene flow between these two isolated populations. In stages 2 and three, environmental differences result in different selective pressures which lead to genetic differentiation. there's mutation happening and the environment is selecting which variants are going to be more favorable in each different environment. And finally,
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when that barrier disappears, the two formerly subspecies have become so different that they can no longer interbreed. They were geographically separated. Now they're reproductively isolated by any of the mechanisms that we've just discussed. Sympatric speciation can occur in animals and plants. In plants, there can be sympatric speciation through polyploidy. This can lead to changes in chromosome numbers causing instant one generation reproductive isolation between the
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newly emerged species and its parent species. One example of sympatric speciation in animals involves the hundreds of species of these fish that are called cichlids that live in Africa's Lake Victoria. What is thought is that sexual selection has led to reproductive isolation between the subspecies. That's been experimentally verified. It's a very complex story. And what I want to encourage you to do is go look at the case study on learn-biology.com. The link is below.
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Here's another mechanism of sympatric speciation in animals. Adaptation to specific microhabitats can also lead to reproductive isolation and speciation such as the evolution of a variety of lice that inhabit different parts of birds. This is kind of astonishing, but there are lice that for example live only on the head of an albatross. And there are different species that live on the
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wings. There are other species of lice that only live on the heads of parrots while others live on the wings of parrots. These are different species and they are in different parts of the bird. And you might say, well, for a little louse, well, maybe that's like a mountain, but that doesn't count as allopatric speciation. There's no geographic barrier. All of these lice are just becoming extraordinarily specialized as they adapt to different parts of these birds and these
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specializations are getting passed on and that's leading to speciation over time. So sympatric speciation in animals because of microhabitat adaptation. What is adaptive radiation? This is a concept that we dealt with earlier when we talked about the evolution of homologous features. Adaptive radiation occurs when one parent species produces several descendant species, each of which has unique adaptations and fills a different ecological niche. The 14 species of
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Galápagos finches shown here, all of which are descendants of a single South American species are an example. This one species arrived at the Galápagos Islands and then radiated into a whole variety of descendants. Each of which has different features, each of which has a different ecological niche. Phylogeny is a reflection of adaptive radiation. Each of the different branches show splitting from a common ancestor. That's adaptive radiation on a very large scale. Finally,
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homologous and vestigial traits, which we talked about in the context of evidence for evolution are also a result of adaptive radiation. It's about splitting from a common ancestor and subsequent descent with modification. We're now going to pivot away from speciation and just look at the evolution of variation and its importance. So, why is phenotypic variation important for evolution?
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Phenotypic variation is essential for evolution. It's the raw material upon which natural selection acts. Natural selection selects for organisms with phenotypes that confer a selective advantage. Remember that the genotype is invisible to natural selection. What natural selection sees, what natural selection acts upon is the phenotype. And the result is that individuals with advantageous phenotypes survive and reproduce at higher rates than organisms with less
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advantageous phenotypes. Now, as those organisms reproduce, they're passing along their genotype, but that's somewhat of a secondary effect. Natural selection acts upon phenotypes. And note that with no phenotypic variation, there can be no natural selection and no adaptation. And that's why loss of variation is so dangerous to a species and can often lead to extinction. So here are a
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couple of examples of the importance of phenotypic variation. Let's start with this one. Explain how variations in phospholipid structure can serve an adaptive function in browsing mammals that forage in snowy environments. Phospholipids, we remember those from unit one. They've got a glycerol with a hydrophilic head and a hydrophobic tail. These are fatty acids over here. Note that these fatty
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acids can be saturated or unsaturated and there can be a lot of variation in that. In mammals that browse in the snow, there is a tendency for the phospholipid tails that are in the body core to be more saturated and those in the extremities to be more unsaturated. Why? Because as the temperature decreases, these unsaturated fatty acid tails keep the membrane fluid so that diffusion can continue
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to occur so that oxygen can continue to flow from the blood into the cells. Whereas the phospholipid tails in the body core are more saturated and that provides a correct level of fluidity in that part of the body. So there tends to be a gradient of more saturated fatty acid tails in the core, more unsaturated fatty acid tails in the extremities. Explain how variation in hemoglobin maximizes oxygen absorption in humans and other placental mammals at various life stages. Let's
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remember that hemoglobin is the protein that transports oxygen in red blood cells in almost all vertebrates. Before birth, humans and other mammals produce fetal hemoglobin. Fetal hemoglobin is a variant and it has a higher affinity for oxygen than adult hemoglobin. Here's the difference. All hemoglobins are the same in that they have these two alpha chains. They're shown in red over here. But adult hemoglobin has beta chains where fetal hemoglobin has gamma chains.
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They're shown in yellow over here. Because of the higher affinity for oxygen, the fetal hemoglobin will absorb. It'll create a gradient that will cause oxygen to flow from maternal blood in the placenta over here into fetal blood. So, here's the gradient. And that of course is highly adaptive because that's how the fetus gets oxygen while it's in the uterus. After birth, developmental genes kick in and slowly the beta form starts to be produced more and more until
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it's completely predominant in the adult. Whereas the gamma form starts to fall and fall and fall. And you can see that that happens even before birth, but the transition is pretty complete 42 weeks after birth has occurred. Explain how variation in chlorophyll types increases the efficiency of photosynthesis. Green plants have two main types of chlorophyll. There's chlorophyll A over here and chlorophyll B over here. And the difference comes down to just a functional group.
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Chlorophyll A has a methyl group over here whereas chlorophyll B has a carbonyl group. Chlorophyll B absorbs more blue light and that's best in indirect light or in shady environments or shady situations. And chlorophyll A absorbs more red light and it's best in direct light. And therefore plants can do a couple of things. One is that there are plants that are shade adapted and other plants that are direct light adapted and those will have different proportions of
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chlorophyll A and chlorophyll B. And then most plants have both. And having both types of chlorophyll increases the amount of light energy that plants can use during photosynthesis over the course of a day or throughout the seasons. Are you asking yourself, "How am I going to get a four or a five on the AP bio exam?" It's 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
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tutorials and interactive AP bio exam reviews. We guarantee you a four or a five on the AP bio exam. See you on learn-biology.com. Phylogeny. What is phylogeny? What is a phylogenetic tree? How are such trees built? Phylogeny means evolutionary history. A phylogenetic tree, also known as an evolutionary tree, is a branching diagram that shows evolutionary relationships. And phylogenetic trees are built using morphological, that means structural, molecular or genetic
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evidence. This is a phylogenetic tree. And one thing that I want to emphasize is that it is a claim that's based on evidence. So the claim here is that hippos and whales are more closely related to one another than whales are to deer. Why is that? Because based on the evidence, which would be morphological, molecular, genetic, hippos and whales have a more recent common ancestor than either does with deer. We'll see the details in the subsequent slides. Define the term clade.
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Clade is an incredibly important biology term that's not known to the general public, but now you'll know it and you'll be able to explain it to people. A clade is a group of organisms that consists of a common ancestor and all of that ancestor's descendants. In this diagram, all of the species and all of the numbered groups are clades. So down here, the large ground finch, that's a seed eating finch in the Galápagos Islands, that's a clade. All members of a
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species have a common ancestor. All humans have a common ancestor. All human beings are a clade. The large ground finch and the common cactus finch have a common ancestor. That's this over here at E. So those two species together constitute a clade. If you go back in time, because there's implied time in any phylogenetic tree, then all of these four species, the woodpecker finch, the small tree finch, the common cactus finch, and the large ground finch, they comprise a
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clade. That's group number five over here. Their common ancestor is this species that's over here at C. Define shared derived character. A shared derived character is a trait that identifies that distinguishes a clade and it evolved in the common ancestor of that clade and it sets it apart from other such clades. For example, lungs and four limbs separate this clade all of these organisms
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that are classified as frogs, lizards, alligators, robins, rats and gorillas that constitutes a clade and they all have this shared derived character. The shared derived feature vertebral column separates this clade that includes all the salmon through gorilla and it excludes the hagfish fur and mammary glands separates the clade that includes rats and gorillas from all the other organisms. These are mammals and those are shared derived features of mammals. What are nodes and
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sister groups? A node is where two branches in a phylogenetic tree diverge. Nodes represent the common ancestor of the two diverging lineages. So at left letters A through E those are all nodes. Nodes show common ancestor. So over here there was a common ancestor that led to the divergence between this clade over here and this species over here the green warbler finch which is not part of
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the clade that includes all of these organisms that have a common ancestor at B. Sister groups are the descendants that split apart from the same node such as the common cactus finch over here and the large ground finch. Those can also be called sister species because that's the taxonomic level at which they're at. So the woodpecker finch, the small tree finch, that clade, that's a sister clade to this clade that's defined by letter E, the common cactus finch and the large
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ground finch. What is an out group? An outgroup is a more distantly related group of organisms that's used to determine the evolutionary relationships among the other organisms in the tree, which is the ingroup. in this phylogenetic tree. A is the outgroup for this clade that's over here at number two. It's a point of comparison for the ingroup and it's a species or it's some other taxonomic
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category that's not part of the clade to which all the other organisms in the phylogenetic tree belong. What's the biggest mistake to avoid in phylogenetic analysis? The misconception that many students naively have is that vertical closeness on a horizontal tree indicates evolutionary closeness, but it doesn't. For example, the frog and the lizard. They're next to one another, but they're not particularly closely related. The only thing that matters on a phylogenetic tree in
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terms of evolutionary relatedness is the recency of common ancestry. So alligators and robins, they have their common ancestor over here. Rats and gorillas, they have their common ancestor over here. Frogs are right next to lizards, but their common ancestor, the common ancestor of the frog and the lizard is all the way back here. And the basic idea is that nodes can rotate. So this phylogenetic tree over here is correctly drawn. It's exactly equivalent to this one over here.
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But you can see that in this one, the lizard is no longer next to the frog, right? So here's a lizard down here. Here's the frog over here. And here's a lizard over here. And here's the frog over here. It's just about rotation. And if you think about the art form called a mobile, mobiles all rotate. It's a kind of kinetic sculpture. And if you can think of phylogenetic trees as one instantiation
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of a kinetic sculpture, you'll have the right idea about this. Always look for recency of common ancestry when you're trying to figure out the evolutionary relationships described by a phylogenetic tree. Define ancestral feature. An ancestral feature is a trait that members of a clade share but which is also shared by larger more inclusive clades. It doesn't define the clade. So for clade G which includes rats and gorillas that's the mammal clade an ancestral
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feature would be claws or nails. And why is that? Because mammals, they do have that trait, but it's also found in this larger, more inclusive clade that runs from lizards down to gorillas over here. Lungs and four limbs is another ancestral trait of rats and gorillas. This mammal clade, it doesn't define the clade, but everyone in the clade has to have that because there's a larger, more inclusive
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clade with that feature. What type of evidence is typically used to construct phylogenetic trees of existing species? Before the 1960s, morphological similarities was what biologists used to determine who was more closely related to whom and thereby construct phylogenetic trees. But more recently, post 1960, remember Watson and Crick figured out the structure of DNA in 1953. Nucleotide sequences in DNA and RNA and amino acid sequences in proteins have become the gold standard in
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determining phylogenetic relationships. So a DNA analysis would indicate that the common cactus finch is more closely related to the large ground finch than to any of the other Galapagos species. That's a hypothesis and you could confirm that through DNA sequencing. What are molecular clocks? Here's how this works. For any specific protein or nucleic acid, the rate of change that's caused by accumulated mutations is constant over time. And if you can calibrate the amount of change
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in a gene or protein to when species split apart, which you can sometimes determine from the fossil record, then you can do two things. One is you can determine a rate of change in that gene or protein, and you can use that rate to determine when other species split apart. What this graph says is it's looking at hemoglobin as a molecular clock based on some fossil evidence. It's basically saying that 20 mutations accumulate every 100 million years. So therefore, if you're
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looking at the hemoglobin between two species and you notice 40 amino acid substitutions, then you could infer that that occurred 200 million years ago. This is widely used in evolutionary biology. It's the basis for claims that for example, humans and chimpanzees had a common ancestor about 6 million or so years ago based on the similarity of DNA between us and chimps. The origin of life. This is one of the coolest topics in biology. For AP biology, you need to master a
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very specific body of knowledge. The key question to address when trying to understand the origin of life is how did life emerge naturally? And this connects to some biology that you've already learned in your AP biology course. For example, you've learned about the cell theory and the idea that all cells come from pre-existing cells. Well, at some point, there had to be a first cell. And in fact, that moment really marks the emergence of life. How did a cell emerge in the
1:05:05
absence of another cell to create it? That's one of the mysteries that we have to contend with in the origin of life. The other one has to do with chemistry. The chemistry of life is largely controlled by complex proteins called enzymes. Enzymes can take simpler substances and make them into more complex substances through processes like dehydration synthesis. Well, how do we get the complex substances that life is based on in the absence of enzymes? What are the
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key steps required to explain the origin of life? The Earth is extremely ancient. It's been around for 4.5 billion years. And life is thought to have emerged about 3.8 billion years. What steps allowed life to emerge? The first thing is that Earth needed to become a habitable and more stable planet. For the first several hundred million years of Earth's existence, it was pummeled by asteroids and comets and all of that needed to come to an end before life could begin to emerge.
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Step number two is about chemistry leading to biology. Biology is based on cells and those cells in turn are based on complex molecules, polymers. The polymers are built from monomers. So how did those monomers emerge? That had to happen abiotically. In the absence of enzymes, monomers had to start to emerge. We need to start to have amino acids, nucleotides, fatty acids, etc. In today's living world, monomers get combined into polymers. How could that happen
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in the absence of enzymes? There needs to be some kind of abiotic process by which that could happen where we have the abiotic synthesis of polymers from monomers and the formation of vesicles. Those are going to become the little capsules into which cells will emerge. In step four, we need to combine those monomers and polymers into those little vesicles to create protocells. These aren't quite living cells the way that we have them today, but they have many of the
1:07:16
characteristics of cells. And finally, we have the emergence of self-replicating cells. That would be the last universal common ancestor over here. And that gives rise to the three great domains Archaea Bacteria. Those two combine that's another story altogether to form the Eukaryotes. The Miller-Urey experiment which was carried out in the 1950s showed that in an abiotic setup without life,
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you could successfully synthesize amino acids in a simulated early Earth environment. Now, as we'll see, some of the details that were involved in the setup of the Miller-Urey experiment were wrong. They don't correspond to our current understanding of the geology of the early earth, but it's an important proof of concept. So what did Miller-Urey do? They created this sterile apparatus with various chambers and tubings and the whole thing was sealed off from the outside
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world and sterile. This chamber over here at number two represented the early oceans. It was heated by a Bunsen burner or some other heating device. And then the steam circulated through these tubes over here. This large area over here is a chamber that represented the early atmosphere. And it was loaded with gases that were supposed to be present in the early atmosphere. And that includes gases like methane, ammonia, hydrogen, and water vapor. Those gases were
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chosen because in the 1950s, that was the current understanding of what the early Earth's atmosphere would be. There are two important points. One is that that was chosen because that was the known atmosphere of some of the gas giant planets like Jupiter and it was thought that that might also be present on the earth. But the most important thing was that no oxygen was present because oxygen was
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produced by photosynthesis. It wasn't present in the atmosphere of the early earth. There were electrodes shown over here at number four by this plus and minus sign. And what they did is they produced sparks which simulated lightning. The gases continued to circulate. They circulated through this condenser over here. And that caused whatever was formed in this chamber here to be caught within this trap. This trap could be sampled without contaminating the apparatus. And
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after a certain period of time, Miller, who was the actual experimenter, it was Stanley Miller. Harold Urey was his graduate thesis adviser sampled the liquid and they found the presence of amino acids. Well, like I said, that didn't necessarily establish that life could be produced in the absence of life, but it did establish that some of the monomers of life could be produced in the absence of life. As I said, some of the details were wrong, but this has proven to be
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the model for many subsequent experiments where there are inorganic catalysts and different mixes of gases that are changed. And in subsequent experiments, the nucleotide bases have been produced, fatty acids have been produced, many of the monomers of life have been produced. So, what's the basic idea? In the absence of life, it's been experimentally established that some of the monomers that make up the chemistry of life could be produced. To understand the origin
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of life, you have to understand the origin of heredity. It's widely thought that RNA, not DNA, was the first hereditary molecule. Why? RNA does store genetic information in viruses. So, it has the capability of being a genetic molecule. But unlike DNA, RNA can also act essentially as an enzyme. RNA can have catalytic properties. It does so in ribosomes where the catalytic part of a ribosome is what actually stitches together amino acids to create polypeptides and then
1:11:25
proteins. We have spliceosomes. We have microRNAs. All of which are catalytic acting upon the world. DNA with its double helical form is fantastic for storing genetic information. RNA because it has both catalytic abilities and information storage capabilities is widely thought to have emerged as the first genetic molecule. Before there were cells, it's thought that there might have been a phase in which there were self-replicating systems of RNA molecules that were subject to
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natural selection that would grow in complexity. And that's called the RNA world that led up to the last universal common ancestor of life. Here's how that might have happened. In the beginning, what we had were inorganic precursor molecules. It's what we talked about in the preceding slide with the discussion of the Miller-Urey experiment. So at some point the sugars, the phosphate and the nitrogenous bases that make up RNA would have to emerge. Those would combine
1:12:33
through abiotic inorganic processes to form RNA monomers. Other abiotic non-enzymatic processes would lead to the next step. And in that next step, we have RNA polymers that start to emerge. They're shown at C. RNAs can fold up into complex shapes and that's what we start seeing over here at D. And those complex shapes can start to have enzymatic properties. One of those enzymatic properties could lead systems of RNAs. It doesn't have to be just one molecule, but there could be a
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system of interacting molecules that could lead the system to replicate itself. At some point those self-replicating RNA systems would become encapsulated within some kind of lipid bilayer and at that point at letter F we have a protocell. Further natural selection further evolution would lead to the emergence of the last universal common ancestor. That's the population of organisms that gives rise to both Archaea and Bacteria and ultimately through a fusion of those two
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domains to Eukaryotes. And if you can look at this diagram, you should pause and test yourself and identify all of the numbered items, then you've learned a lot of cellular biology and you're well on the way to being set up for success on the AP bio exam. Just to run through at number one we have a lipid bilayer. Remember it doesn't have to be a phospholipid bilayer because Archaea have
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a different kind of bilayer structure. At two we have DNA being the genetic material that's found in all living things. At three we have RNA which is used for information transfer and other things. At four we have ribosomes which are translating messenger RNA into protein. At five, we have a membrane channel that's allowing matter and energy to flow in and waste to flow out. At six, we have
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complex proteins that are acting as enzymes which are combining monomers into polymers through dehydration synthesis and then pulling apart those polymers through hydrolysis. And at seven we had ATP synthase which is using a flow of protons across the ATP synthase channel to generate ATP that universal energy molecule from ADP and phosphate. That's the last universal common ancestor and that's what you need to know about the origin of life for AP biology. Here are your
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