शैडोइंग अभ्यास: How evolution works, in 54 minutes | Sean B. Carroll: Full Interview - वीडियो के साथ अंग्रेजी बोलना सीखें
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How can all the diversity and sort of seeming order that's out there in the world
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emerge from a process dependent upon chance?
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It kind of works like a staircase.
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Chance invents and natural selection propagates that chance invention.
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Our immune system works on the very same principles of mutation and selection as evolution at large does in the big world.
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cancer is truly an evolutionary disease meaning that it is a disease
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that results from the exact same evolutionary process we're describing so
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while darwin's is the most famous figure associated with the theory of evolution alfred russell wallace played a key part
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and in their day this was referred to as the darwin wallace theory i'm sean b carroll evolutionary biologist
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and author of several books including my most recent a series of fortunate events chance
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and the making of planet life and you chapter one how life works the staircase of evolution
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so evolution what it really means is change over time
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so we want to know how that change occurs over time
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and there's two dimensions to this process and it kind of works like a staircase
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and one process is mutation and that's the rise in the staircase those occur by chance
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if mutation didn't happen all things would be identical
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so you need mutation to make individuals different from one another those mutations are genetic changes changes in their DNA.
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If by chance that changes a property that favors reproduction, survival of the individuals, it will spread.
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And that's the selection process.
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And that's sort of the run in the staircase.
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Chance invents and natural selection propagates that chance invention.
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And once that process has happened, new mutations can then be added on top of that, maybe even changing the character a little bit further.
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And that's another rise in the staircase.
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And if that's working better, that's going to spread.
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And so it's the cumulative set of mutations and the cumulative process of selection that takes us up that staircase.
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So that staircase could have goodness knows how many stairs, but it has to go through this stepwise process of individual mutations arising,
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sweeping through the population, new ones arising, sweeping through the populations.
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It doesn't go from the base of stairs to the top of the stairs in one jump
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and this is hard for people to get their heads around
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because they may think about that first step
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and it's sort of hard to imagine you know how do
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you get something as complicated you know as individual organs like an eye
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or a wing of a bird or things like that
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but time immense time the speed with
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which some new adaptation spreads through a population depends upon the magnitude of the advantage it conveys
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if it's about a three percent advantage, meaning that about 103 individuals survive for every hundred that don't have it.
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Well, that will take about a thousand generations to spread through the population.
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Now, I'm saying generations because it depends upon the generation time of the creature.
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So if the generation time, for example, of humans is 25 years, it'll take 25 ,000 years for that to spread through the human population.
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But if the generation time is 20 minutes, you can work it out.
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It'll take 20 ,000 minutes to spread through, which is much shorter.
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It's a matter of generations because its reproduction is a generation -by -generation process.
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It's really important to underscore
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that these mutations occur at random without any consideration of whether they're good or bad for the organism.
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It's the external conditions that are going to sort this out.
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So some things can be good for one creature and bad for another.
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So, for example, a color change might make a creature more invisible in some settings, more visible in another.
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Some mutation may make it better adapted to warmer climates, less well adapted to colder climates, right?
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So it depends on these external circumstances.
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So the mutations arise at random.
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Well, what about those external circumstances?
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What we'd say is the abiotic conditions, whether the physical world that the creature is living in.
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Well, that's also generated a lot at random.
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Tectonic plates moving across the earth,
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um, you know, volcanism, all the things that shape conditions of life are often due to physical processes of the earth.
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Of all the many thousands and millions of things that creatures have come up with, I have a few of my favorites that I think really exemplify this process of adaptation.
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And one of my favorite sets of creatures are some fish called ice fish.
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They live in the Southern Ocean around the Antarctic
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and they live in water
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that is actually below the freezing temperature of fresh water they're
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right around about 29 degrees Fahrenheit is the ocean around the Antarctic and that's a challenging environment,
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so challenging, for example, that you may know that there's ice flows around there.
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And if little ice crystals just get into the bodies of these fish, they'll nucleate freezing.
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They'll freeze like fish sticks.
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So they need to have a mechanism that prevents them from freezing at that cold temperature.
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And what they've done is they've evolved antifreeze.
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Certain proteins in their bloodstream made in very large quantities suppress the ability of ice crystals to grow inside their bodies.
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And so they're able to tolerate that sub -freezing water of the Antarctic.
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And other fish aren't.
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So what's happened over the last 30 or 40 million years is
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that a lot of fish that once swam in those oceans, sharks and rays and all that, they're all gone.
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They're extinct from those waters.
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We find them in more temperate waters.
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But it's the ice fish and the antifreeze -bearing relatives that exploit those waters.
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And the ice fish have also come up with something that's incredibly nifty and shocked naturalists when they first discovered it, which is if you open, which any fish you know,
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slice it open, you're going to see red blood because that's something
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that animals with backbones have and have had for almost 500 million years on this planet.
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But you slice open an ice fish, their blood is colorless because they've gotten rid of red blood cells.
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So they don't even have a mechanism for carrying oxygen actively in their bloodstream like we do.
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They've ditched red blood cells and the reason they've ditched red blood cells is that those low temperatures, it makes their blood too viscous and that's a disadvantage.
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To the ice fish, it was an advantage to get rid of red blood cells.
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To the rest of us, it's instantly fatal.
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So it's a good illustration of just how conditional these adaptations are, that to exploit the resources of the Southern Ocean, you've got to make antifreeze
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and get rid of your red blood cells where the other parts of the world antifreeze would be irrelevant
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and your red blood cells are necessary for every second of life let's talk about speciation
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that process of variations helping to adapt that's the process of adaptation
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but speciation is the generation of two species from one what is what does
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that take for there to be two to two species to form
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and we know this is where the island biology of Wallace
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and Darwin help is that they were seeing species on different islands.
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Well, islands provide some isolation, and that isolation means that those populations aren't exchanging genes.
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Over time, each of those populations will accumulate mutations that exist in one population and not the other, vice versa.
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Well, those can become genetically distinct enough that if those things were ever to come back again in contact, they may not be compatible with one another and they'll be species.
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So how long does that take?
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Well, it's been estimated for big animals like mammals and birds, that works out to roughly be about two million years.
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But two million years is still a long time.
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And you've probably heard, for example, that there's now very strong evidence that Homo sapiens, our species, mated with Neanderthals,
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a distinct species and what's really happened in the last few decades is
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that for biologists
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that species barrier has become much more porous than we first
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thought it was in the old days in darwin's day species were characterized as really distinct things
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and we didn't think there was any kind of
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shenanigans going on between them but we now understand
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that it's a it's a much more porous situation
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that for some period of time as populations are diverging they can get back together
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and things that we humans might call distinct species can often interbreed another common question
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or idea is is that you know for example
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if humans evolved from apes why are apes still around well the important thing is understand
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that evolution is a splitting process so the family trees keep splitting
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so the human part of
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that tree has had now its own separate history from the eight part of
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that tree we shared a common ancestor about six million years ago but apes have gone on living as they do, for example, in the old world.
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And there's a great diversity of apes, of course, still here, baboons, orangutans, gorillas, chimpanzees, et cetera,
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while the human branch has gone on and has its own evolutionary trajectory.
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It's not that evolution is linear and that everything new replaces the old.
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It's a splitting process.
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And so that's why the tree of life has just split into enormous numbers of branches from common ancestors.
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Two of our main records of evolution are the fossil record and the DNA record.
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The DNA record is largely only accessible to us for living creatures
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and maybe some creatures that have lived over the past million years you know, do we have every brick?
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Do we have every intermediate?
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No, because extinction takes away 99 .9 % of all species.
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So if there was no extinction, we'd have a perfect record of evolution, right?
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We don't have the DNA record of dinosaurs, for example, but we've got the fossil record of dinosaurs.
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So we use these two records to sort of reconstruct the history of life.
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That allows us to reconstruct the evolution of things that are fairly complex.
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Let's take something like a walking limb from a fish fin.
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This evolutionary process transpired over 20, 30 million years, about 380, 390 million years ago.
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To do that, we have to get fossils
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that represent the various stages of evolution
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and see how did all the bones change so you went from a swimming fin to a walking limb.
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And the fossil record by now is pretty darn good.
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Then we can go to creatures that have fins, fish, and we go to creatures like amphibians that have limbs,
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and we can figure out how do those genetic programs work and where are the differences.
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Now, we don't have every detail sorted out, and that would be incredibly time -consuming and expensive to do,
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but we certainly have the general picture that we understand how the bones changed in history,
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and we understand how the development of program changed to generate a limb in the place of a fin.
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And that's not something Darwin ever had.
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That's something that we really only had for the last 20 to 25 years.
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So evolutionary science keeps building on this huge foundation.
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And what we get is an ever more detailed and ever more confident record of what's happened.
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But what's it no doubt is that this process,
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mutation and selection, mutation and selection is the universal going on in every population of every living thing
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every day in fact this process of mutation and selection seems
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so universal that we think it must have played a vital role at the origin of life
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and that anywhere where life exists in the universe it's operating
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so evolution is this vast and rich process
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and you know we've been trying to understand it for 160 years
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and in the course of that there's some misunderstanding and just how it's communicated,
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where I think there's some conflict between the terms we scientists use and sort of their common understanding.
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And one of those is theory.
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We talk of scientific theories.
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Theory is much higher on the hierarchy than, for example, a fact or just an observation.
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A theory is assembled from lots and lots of facts
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and independent lines of evidence that sort of cohere
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so a theory is really sort of the top category of
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scientific idea of course you know in the street theory might mean that's my best guess
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or that's just something that i'm conjecturing
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the way we talk about those kind of conjectures we call those hypotheses
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and that when hypotheses have been rigorously tested that's what can contribute to making
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a theory so folks when we speak of theory think that we're still very tentative about the truth of evolution.
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That's not all the case.
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The theory of evolution, which has grown enormously in the last 160 years, is a huge body of observations,
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evidence, and facts that are consistent with one another, that come from completely different sources of science.
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And that's what gives it its power.
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We, of course, wish that maybe that connotation of theory that's you know, more of the everyday connotation would be better understood.
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Chapter Two, How Our Bodies Work, The Staircase of Self -Defense.
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Now here's something about the staircase of evolution that's very little appreciated.
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It's going on in every one of our bodies every day.
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It's keeping us alive.
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and that's because our immune system works on the very same principles of mutation and selection
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as evolution writ large does in the big world every day
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we are exposed to all sorts of potential pathogens bacteria viruses fungi parasites we've got to fend these off
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and by the time we're full grown adults,
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there are actually more bacterial cells living on and in our bodies than there are our own cells.
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Trillions and trillions of microbes.
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We've got to keep these in check or of course we'll suffer and potentially die.
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And that's the job of our immune system.
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And our immune system operates on the very same principles as the staircase of evolution it's a staircase of self -defense.
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And the most remarkable property of our immune system is it
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seems to be able to recognize as foreign virtually anything that can come at us out of nature, including entirely new pathogens that didn't even exist.
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in the human population.
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And how do we do that?
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Well, it involves a process based on mutation and selection.
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And the way this starts, I'll just describe it starting with a single cell.
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So you have billions of cells, but these cells have different molecules on their surface that when they are complementary to molecules on the surface of a pathogen,
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they're activated, they're engaged.
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And when engaged, they multiply very rapidly such that over a period of about a week, one cell may become billions of cells
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and start to pump out large quantities of chemical weapons known as antibodies that thwart that invader.
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These billions of cells of our immune system are actually clones, clones that are subtly distinct from each other,
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that have unique ability to recognize something else.
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Now, that something else could be any variety of things on an invading pathogen.
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But once they recognize that, that clone gets amplified, can grow to be many, many, many cells in the course of a week or so.
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That first wave of defense is decent, but not optimized.
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There's actually a mechanism to make those chemical weapons, the antibodies that cell makes even more potent,
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even more deadly to essentially the invading pathogen.
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And that's because there's a specific genetic mechanism that mutates the antibody encoding genes, leaves the rest of the genes in the body alone.
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Just the antibody genes start undergoing a process called hypermutation
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and therefore generating all sorts of antibody variants and the antibody variants that recognize the pathogen better are selected for.
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So here we go.
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We're climbing the staircase.
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So this hypermutation process, you now select antibodies, and this can go through various cycles to make ever better and better antibodies.
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So we're really zeroing in on this particular pathogen.
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So late in immune response, say for example, the second week you're recovering from a flu virus,
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your immune system is ever more potent ever more ever more powerful in defeating its enemy
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because it's up that staircase eventually a staircase sort of splits
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and some cells are set aside so it's called memory cells
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they're there to be used
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when this pathogen is encountered again other cells continue to make
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the antibodies now this is the marvelous thing y 'all are familiar with a phenomenon where for For example, you don't get measles twice.
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You don't get chicken pox twice, et cetera.
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Why is this immunological memory?
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That even if 50, 60, whatever number of years ago you might have been exposed to that virus,
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your immune system is still poised to attack it again if you're exposed again, so you don't even get the infection.
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This system is called adaptive immunity, much like the process of evolution of mutation and selection is adaptive.
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It really only exists in this form in animals with backbones, long -lived, generally larger animals.
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And you can see its utility because the longer your lifespan, the greater the chance you're going to re -encounter a particular pathogen.
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If you're a short -lived mayfly or something like this.
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You don't live long enough to see the same thing twice.
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There's not that kind of immunity.
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So lots of animals, including simpler things like worms and flies and all that, they have what we call innate immunity.
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They have ways that sort of put barriers up against pathogens.
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But this adaptive immunity only exists in creatures with backbones,
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with vertebrates and it's pretty elaborate in in us in in mammals animals with fur etc
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but it's pretty well developed even in things like fish
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and sharks inside our bodies the time scale of this process
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is very very fast it's more like what we described with respect to microbes
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because it starts with cells and cells that can multiply pretty frequently
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so a lot of evolution can take place in a short time most of us are sort of familiar
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that you know most infections don't knock us down for more than about a week that's
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when our immune system eventually sort of catches up
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and overtakes the pathogen so
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that gives you a sense of the time scale it takes to mount the response expand
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that response to the point where it overwhelms the pathogen whereas
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out there in the world sort of a battle between predator
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and prey or whatever
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that may go on for hundreds of thousands of years before
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there's sort of a winner same process much more rapid time scale in your body how is it possible
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that we can recognize virtually anything that the world will throw at us.
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And fundamentally, one of the problems there is sort of a coding problem.
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how can one make all the different kinds of antibodies that could recognize all the different possible pathogens that, you know, a species might encounter?
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And the solution to that required understanding how antibody genes are encoded in DNA,
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something we weren't able to do until the 1970s or so.
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And what that's revealed is that we mix
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and match pieces of antibodies in a way that we can generate millions of combinations of antibodies.
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And it's now estimated that we may be able to make about 10 billion different antibodies.
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And you might go, well, that sounds sort of impressive, but okay.
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Well, here's the thing.
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In our entire genome, all of our DNA, we only have about 20 ,000 genes.
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So how do you make 10 billion antibodies when there's only 20 ,000 genes to begin with.
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And this is the brilliant trick of the immune system.
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It makes antibodies from short little gene segments that it mixes and matches in millions, if not billions, of combinations.
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So the trick of combinations is that it's just like in a, you know, if you can take a deck of cards, right?
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And you have five cards you draw from a deck.
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there's lots and lots of different combinations you can, even if you have only 52 different cards.
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And so from a modest number of antibody genes on the order of a few hundred, by mixing and matching them in pieces, we can generate enormous numbers of antibodies.
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So the immune system, even with all its powers, can still be sort of beat to the punch.
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There's still pathogens that can kill us.
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And this is why we vaccinate.
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And we understand in vaccines, generally what we're giving is a little component usually a non
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-living component not the virus itself not the pathogen itself
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but maybe just a molecule that represents that pathogen and we're using
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that to prime the immune system so we're activating the immune system
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so it goes through some of those steps on the staircase establishes memory
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and is poised to respond should we encounter that pathogen and by being vaccinated by being immunized that can save lives
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certainly save the suffering of any of a particular disease you
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know shorten its course save us days off work whatever it might be
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but this is why we have these vaccine strategies and we seek ways
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to give our immune system a head start because
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if we don't vaccinate then we're at risk of suffering the damage
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that pathogen causes unless or until our immune system catches up feeling lousy
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or in some cases there's lots of morbidity with these infections
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one of the most notorious ones in human history is the smallpox virus
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which killed hundreds of millions of people in human history
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and even tens of millions of people in the 20th century until we came up with a vaccine.
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And there was a global effort to vaccinate virtually every human on the planet.
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And that eradicated smallpox from the world so that now we don't even vaccinate for smallpox.
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But that was a virus that moved faster and caused greater pathology than our bodies could keep up with.
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So we understand this evolutionary process is what drives our adaptive immune system and protects us against enemies from without.
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But it turns out that sometimes the enemy is coming from within the house.
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And I'm speaking specifically of cancer.
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And cancer is truly an evolutionary disease, meaning that it is a disease
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that results from the exact same evolutionary process we're describing of the evolutionary process in the external world, of the evolutionary process in the immune system.
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Cancer forms in the same way and that is mutations take place in individual cells
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that if they convey some growth advantage to those cells,
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those cells may outgrow their neighbors and additional mutations may happen so they outgrow their neighbors further.
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And that's what we define as a tumor, a population of cells that is now growing unregulated relative to its normal neighbors.
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And that's a threat because that unregulated growth can lead to spread throughout the body, can lead to organ involvement, etc., and death.
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But the other concern is, as that cancer gets larger, some of those cells are going to get yet additional mutations.
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And some of those cells are going to get yet additional mutations.
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And so as cancer progresses over time,
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that tumor is less and less like the cell it started from and the tumor itself is more genetically diverse.
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And that's giving us a real challenge therapeutically.
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So there is a staircase of cancer.
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And the way to understand that is that our risk of cancer is really age -dependent.
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The incidence of cancer goes up really significantly as we get older.
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And think for a moment why that might be.
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And what that is, is it takes time to climb that whole staircase.
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So, later in life, individual cells have gone through more divisions, they've had more chances to accumulate mutations,
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mutations that give them some growth advantage over other cells, and so our risk of cancer grows really significantly as we get into our 40s, 50s, 60s, and 70s.
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So that tells us, not only is it an evolutionary disease, it's a genetic disease.
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It's mutations taking place in genes that somehow disrupt the normal process of controlling
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cell growth
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so a huge interest has been what are those genes how
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do we find them how does this all work we first got a hint
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that cancer was a genetic phenomenon
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when scientists first started seeing chromosomal changes in cancers chromosomes
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that were broken infused and things like this and
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that all the tumor cells would have those broken chromosomes
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or tumors that arose independently in different people would have those rearranged chromosomes
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and that gave us a hint okay something genetically is going on
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but the crucial thing was to identify well what genes well thanks to
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genomics thanks to gene cloning we now know
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that there are about 20 000 genes that essentially run the human body
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and we've identified about 150 of those that
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when mutated can contribute in some way to cancer we'll call those drivers
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and those drivers split into two classes one class
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we'll call accelerators because when they're mutated they really accelerate cell multiplication
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they also have the name oncogenes promoting cancer another class of genes they serve as brakes they hold back proliferation
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but if they're disrupted by mutation and we no longer have their braking function
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and the cells can grow out of control
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so just like an out of control car out control cell proliferation can be due to a stuck accelerator or broken brake.
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It can be due to oncogenes that promote cancer or tumor suppressors would normally suppress that cancer, but they've been disrupted by mutation.
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So scientists have banded together across the world to build this sort of catalog of driver genes.
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And so they study the state of these genes and all sorts of cancers.
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And there's some really, really clear insights from doing this.
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And the first is, well, it's a multi -hit process.
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Usually any cancer has disruptions to multiple genes, might be three, four, five, even seven of these driver genes.
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And if we look at cancers that arrive in kids and compare that with cancers that arise in adults, there's a really profound distinction.
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when we look in kids we see there are very few mutations overall in the dna of the cancer cell
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but they'll be in driver genes you don't see many other mutations
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that have taken place that are different say from mom
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and dad's dna and that's because a young child its cells have not gone through
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that many divisions it's not accumulated very many other mutations it just
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so happens the mutations that occurred were in these critical driver genes it's horrible heartbreaking bad luck But the longer we live,
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all of our cells, whenever DNA is copied, mutations occur.
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Now, most of those mutations have no effect.
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They're sprinkled among the billions of bases that we have.
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But every now and then, one of these driver genes gets hit.
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Well, the longer we live and the more divisions our cells have gone through,
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the greater the chance that there have accumulated mutations and eventually hit one or more driver genes.
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And once they hit a driver gene, if that cell starts to outproliferate its neighbors,
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well then those cells in turn may be going through more rounds of division, more mutations.
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And so now essentially the snowball is rolling such that by later in life,
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we have cells that have accumulated a number of driver mutations.
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And many of our cells at least have one driver mutation.
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It may not be pathogenic whatsoever, but a lot of our cells will have mutations in them, some of which could eventually be a problem.
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So understanding that cancer is this sort of disease, this interplay of mutation and selection, there's really three factors that can contribute to the formation of cancer.
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First is just bad luck, that the small number of mutations that are going to happen anyway just happen to hit driver genes.
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Really, that's the explanation of pediatric cancer and
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And the kindest thing you can do to any parent whose child is struck is to reassure them
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that there was nothing they did to cause it and nothing they could have done to prevent it.
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Then there are lifestyle issues like tobacco use and sun exposure.
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They'll increase the risk of particular cancers.
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Lungs, because that's where the smoke goes.
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And of course, the skin, because that's what's being exposed to the sunlight.
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And the third is just age.
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It's time.
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The longer we live, the more divisions our cells have gone through, the more mutations have happened.
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And the more all the environmental things that we've been exposed to have had a chance to work on us.
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So that later in life, our cells are carrying lots of mutations And we just hope
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that none of those cells have sort of that unlucky combination of mutations that will make it an uncontrollable tumor.
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So I think there's a few pillars of how we're combating cancer now that's really different from how we did it before.
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Now, for prevention, we're looking for these mutations.
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So you've seen, for example, a product like Cologuard, where a stool sample can be sent to a company.
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Well, they're looking for mutations characteristic of gastrointestinal cancers in that fecal sample.
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Okay, so that's early detection.
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And we know that the earlier you can detect cancer, the better shot you have of counteracting it.
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The second pillar is to know those cancers and to realize that different driver genes are mutated in different cancers.
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So instead of treating breast cancer as a monolith,
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we now subtype breast cancer according to the mutations that exist in an individual's tumor.
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So it's really important that the genotype, meaning the genetic makeup of a tumor, is analyzed when that is first diagnosed.
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That will shape the treatment course, because the other thing that oncologists are doing is they use different drugs,
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different regimens to go after these cancers is to study which things work against which genotypes of cancer.
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So we're now, I think, classifying and categorizing cancers with much greater degree of sophistication.
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Then there is the specific therapy side.
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All sorts of drugs have been designed to go after those mutated genes.
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So to specifically target what has gone wrong in an individual cancer because of the mutation of a particular gene.
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Some of these drugs have been spectacular success, some are doing a good job at let's just say buying time in the hope
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that the cancer can be contained
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and you know managed over a longer period of time and treated more as like a chronic disease, not necessarily eliminated, but at least managed.
382
Only in the last about 25 years has this really been possible, but the practice of this has really grown enormously in the last about 15 years.
383
And there's all sorts of new drugs under clinical trials at any given moment.
384
Again, trying to give a much more specific therapy to the particular alterations that have happened in a given individual's tumors.
385
Better prevention, better diagnosis, better therapy.
386
This is driving cancer rates down, certainly for certain types of cancers, and hopefully going to drive survival rates up over the long term.
387
These parallels in how life evolves, how the immune system works,
388
how cancer arises, they're, at one level, they're startling because the connections aren't so obvious,
389
but fundamentally they're operating on the same process, this mutation and selection.
390
But of course, mutation is a random process.
391
And it's really hard to get our heads around how can all the diversity
392
and sort of seeming order that's out there in the world emerge from a process dependent upon chance.
393
Yet, there you have it.
394
Whenever you have variation and you have competition,
395
natural selection operates and gives us the variety of life.
396
In the immune system, chance is being exploited.
397
You think, well, we can't leave the defense of our bodies against chance, but here we're exploiting chance.
398
Now, of course, cancer has its root in chance, the unlucky mutation that hits a gene that could throw a cell out of balance with the body.
399
That evolutionary process we've been discussing is one of error and trial, whereas humans sort of think like engineers,
400
that we think of what we want as an outcome and how we can get there sort of in the shortest distance.
401
And we may use some trial and error, but we really try to minimize the error, whereas really these evolutionary processes start with error.
402
They start with a random change and then try those things out.
403
and it's i think it's just been hard for us to get our heads around
404
that yet the more we understand this and all of us manifestations, and the immune system and cancer are two later realizations,
405
we see that this process is a fundamental biological process,
406
random genetic variation and the sorting of that variation through natural selection.
407
Chapter four, the untold story of Alfred Russell Wallace.
408
so about 15 years ago on a visit to the university
409
of cambridge i happened to visit the archives there where they hold a lot of original materials from darwin
410
and to my astonishment they brought out
411
and placed into these sweaty hands a copy of one of the early manuscripts
412
that many many many years later would be modified into the origin of species after darwin got back from his voyage
413
He was pondering these ideas, and he decided to write them down in essay form.
414
And by 1844, he completed a 230 -page essay that fleshed out a lot of his basic ideas.
415
He wouldn't publish anything on evolution for 15 years.
416
That essay, I think, was lost for decades and found under the steps of his house.
417
So when it was presented to me, all over the manuscript, including on the back pages, there were drawings by Darwin's kids.
418
They had been using it like scrap paper.
419
It was a spine -tingling moment for me
420
because this was really the birth of one of the biggest ideas humans have ever had.
421
And I'm grateful that they found it under the stairway at Darwin's house.
422
So while Darwin's is the most famous figure associated with the theory of evolution, Alfred Russell Wallace played a key part and deserves huge credit,
423
both for his ideas and for his enormous effort.
424
So really important to understand that the prevailing idea at the time to
425
which Darwin subscribed and most British scientists subscribed was what we'll call special creation or the theory of special creation.
426
And that was the idea that every species was specially created by God and sort of placed,
427
or at least emerged, in the habitat or in the place on the globe that best suited it.
428
Now, what started to shake that theory in Darwin's mind and in Wallace's mind was in the course of their journeys,
429
particularly when they visited archipelagos, strings of islands.
430
Each of them observed species on different islands that were slightly different from one another.
431
Now, Darwin, this is just a twist of his story.
432
After nearly five years at sea and having made a full voyage around the world, they were about to turn from the southern tip of Africa back up to Europe.
433
But his captain, who was sort of obsessive, decided he wanted to do some more measurements in South America, so he went back across the Atlantic.
434
And Darwin was at first just crestfallen that he wasn't headed home, but he needed to make good use of that time.
435
And he started to take his notebooks out and review what he had seen, but also sort of annotate them.
436
And he thought back to the Galapagos Islands, and he thought back to these mockingbirds that had seen on different islands.
437
And he saw that on different islands, the mockingbirds were slightly different from one another in their feather patterns and things like that.
438
And he thought these islands were within sight of one another, just 50 or 60 miles away from one another.
439
If a creator was placing species sort of perfectly adapted to each place, why would these mockingbirds be just slightly different from one another?
440
Now Wallace's story is almost is more dramatic because Wallace, after four years in the Amazon,
441
really at the breaking point, decided to return to England with specimens and whatever ideas he had collected.
442
And on his way home, his ship caught fire.
443
He had to get into a lifeboat.
444
The ship sank right in front of him with all of his specimens.
445
And he was in an open lifeboat for 10 days, hoping to be picked up.
446
And he was picked up, eventually made his way back to England.
447
You'd think after that experience, he would have sworn off all voyaging.
448
But two years later, he goes back out
449
and does an eight -year voyage across the Malay archipelago and collects tens of thousands of more specimens.
450
He noticed, for example, the bird -winged butterflies.
451
These beautiful, incredibly brilliantly colored large butterflies were slightly different from island to island.
452
They both thought, in the theory of special creation, these islands all looked alike.
453
Why would there be just slightly different species island to island?
454
And it struck both of them because species could change.
455
Species weren't stable.
456
They weren't immutable, as the theory of special creation argued.
457
They, in fact, changed.
458
And this opened up the big question then, or at least the daring question, of...
459
are species the product of natural processes or divinely created
460
and they thought this was strong evidence
461
that species change naturally they change according to the conditions they encounter in different places
462
and the islands were crucial sort of laboratories for understanding this because
463
the volcanic islands of the galapagos look very similar to one another
464
but the creatures were a bit different the islands of the melee archipelago very similar foliage
465
and all that but the creatures were a little bit different.
466
And the only way they could sort of reconcile that was to say, well, the species were changing.
467
They weren't fixed.
468
They weren't immutable.
469
And as they worked further, they thought about some other patterns.
470
They knew about fossils.
471
In fact, Darwin discovered some really interesting fossils on the coast of Argentina.
472
And through correspondence back home, while he was at sea, he realized these were sort of larger versions of animals that lived in South America at the time.
473
So he found, for example, giant ground sloths, huge, like eight feet tall ground sloths, much larger than the living ones.
474
But he realized, hmm, those are extinct creatures.
475
What's the relationship between the extinct and the living?
476
He's starting to think about that genealogy between the extinct and the living.
477
And Wallace is also becoming aware of these fossils
478
because he's reading now what's coming out from the first studies
479
of fossils in Britain in the first part of the 19th century.
480
They had also each read this work by an economist, Thomas Malthus.
481
And Malthus emphasized that there were limits on populations.
482
He thought about the growth of populations.
483
And Malthus said that disease and famine, that limited, for example, the growth of populations.
484
Well, Darwin and Wallace, being out of nature, they understood that life was very tough.
485
They understood that really life was a battlefield, a contest, and that far more young are produced than can survive to adulthood.
486
And what's uncanny is when you look at the writings of each of these individuals, Darwin's notebooks, Wallace's draft manuscript,
487
they use the same language.
488
They describe life as, quote, quote, a struggle for existence.
489
Exactly the same words, unbeknownst to each other.
490
And they talk about variations, however slight, and that they could be favored.
491
And that led Darwin to coin the word natural selection.
492
They'll be selected for in nature.
493
And the things that are disadvantaged will be selected against.
494
And Wallace said essentially the same thing, that one could imagine if there's a slight advantage
495
that slight advantage will be passed on generation after generation
496
so darwin for 20 years is back home in england he's well known
497
because right after he did the voyage on the beagle he wrote a book
498
that we call today the voyage of the beagle
499
and it was a popular read it's a great read it's still a great read today about his travels
500
and he was an eminent naturalist.
501
Wallace was an unknown.
502
He was from far more modest upbringing
503
and he was really paying his way on his voyages by selling a fraction of the specimens that he was collecting.
504
So he was thousands and thousands of miles away from the center of science in England
505
and he wasn't connected really at all.
506
So Wallace by 1858 has a pretty good idea that life changes, life evolves.
507
And he writes up a very short account of his thinking about how that works.
508
And he decides to send it to the one naturalist with whom he struck up a correspondence who thinks might appreciate it.
509
He sends it to Charles Darwin.
510
Well, this event rocks Darwin because Darwin has not gone public with his theory of evolution.
511
And now here's this far away correspondent, 7 ,000 miles away from England, who in just a few pages has essentially the same idea that Darwin has,
512
that Darwin's labored on for about 20 years.
513
Well, Darwin's friends rally and decide
514
that the best thing to do would be to read Wallace's paper
515
and an excerpt from Darwin's work in front of a British
516
scientific society to sort of put both of these ideas out in the public.
517
Darwin wasn't there.
518
It turns out Darwin had suffered tragedy.
519
He was burying his Charles Jr., one of his sons, on the day this paper was read.
520
And Wallace was 7 ,000 miles away, didn't even know it was going on.
521
It really didn't make much of a splash.
522
Not much attention was paid.
523
But the next year is when Darwin published on The Origin of Species, and that's when everyone paid attention.
524
The response and acceptance or rejection, particularly.
525
to Darwin's Origin of Species because that's the book everybody could put their hands on.
526
It sold out in its first printing.
527
It was reprinted quickly.
528
It was translated into other languages.
529
American versions were made.
530
So people who are interested in science, biology, natural history around the world could get their hands on Darwin's ideas.
531
So the reactions were a very wide spectrum.
532
Thomas Huxley, who was one of Darwin's close confidants, sort of thought, you know, wow, why didn't I think of that?
533
He thought it was, you know, compelling and sort of obvious.
534
But I think one thing to appreciate with Darwin is that his book is extraordinary in that he also
535
presents and analyzes the critiques of his own theory.
536
I mean, imagine that this is just something that human beings don't generally do.
537
If they've got an idea, they're going to put out all the evidence in favor of their idea,
538
and they're usually not going to present to the opposition all the evidence either against it or all the evidence that's missing.
539
But Darwin did this in a masterful way and basically often saying things like, you know, if something, if a particular thing was found, it could crush my theory.
540
Or if my theory is true, this would be true, but there wouldn't necessarily be any evidence weighing on that.
541
So it was a masterful presentation.
542
And I think that gave, it made it very accessible to people.
543
They understood the strengths and weaknesses of the theory.
544
And then new discoveries could be interpreted in light of that theory.
545
And as some new discoveries, particularly from the fossil record, came to light, well that gave a lot of power to Darwin.
546
Because Darwin at the time Origin of Species was published, the fossil record was pretty skimpy.
547
But Darwin made some really strong predictions about what should be found, for example, in the fossil record.
548
And one of those was transitional forms.
549
If the tree of life has evolved in the way that he said, there should be forms that are intermediate between existing forms today.
550
And two years after the origin of species, a fossil called Archaeopteryx, which has got mixed characteristics of both birds and reptiles, was discovered.
551
And I mean, you couldn't have drawn anything better than that fossil for supporting Darwin's theory.
552
So I think the reception of the scientific community, some of it at first was, you know, positive, but there were long, long holdouts.
553
There were career -long holdouts against Darwin among even very eminent natural historians, biologists, and scientists.
554
And that holdout was really for reasons we'd all recognize today.
555
While Darwin didn't, in 1859 didn't comment directly on the evolution of humans.
556
He did later in 1871.
557
Everyone knew that humans were going to be a touchy subject because for at least a couple millennia,
558
the thinking was that man was created in God's image, not descended from some previous animal forms.
559
But clearly Darwin's theory would be interpreted to say that no, humans, just like every other animal,
560
evolved their anatomy and their physiology from pre -existing forms.
561
And some scientists held out on that point, both perhaps from their own viewpoint of faith,
562
but also, I think, because of some pressures in the academy.
563
Darwin was on the short list to be knighted.
564
When the origin of species came out, well, he never got that knighthood.
565
So, you know, This was an idea that many people found repulsive.
566
They were really worried about the societal implications to sort of
567
take the creator out of the immediate picture of sort of tending to human affairs.
568
And that's, of course, still a struggle that exists today.
569
And scientists being part of society, it was not universally accepted,
570
far from it where Wallace really finally grasped the scope of what Darwin had been working and thinking
571
was in 1859 when The Origin of Species was published
572
and he got he received a copy of The Origin of Species
573
and he read it
574
and re -read it in fact Wallace's own copy is in the Natural History Museum in London
575
so we can understand sort of his reactions in real time
576
But I think one of the most poignant things I know in the history of science
577
was Wallace's put his thoughts and reactions in a letter to his close friend and confidant, Henry Walter Bates, with whom he had first traveled to the Amazon.
578
And Wallace is just gushing with admiration for Darwin.
579
And he says, I never, given any amount of time, I could have never come up with something as massive and compelling as Darwin.
580
And he said, I don't think any branch of science has ever been created by an individual such as this, such as Darwin.
581
So, Wallace was in awe of Darwin's synthesis, which was the origin of species.
582
But they were mutually generous to each other.
583
Darwin, right off on page one, acknowledges Wallace and Wallace's ideas.
584
And Wallace later, for example, when he writes his first major book, he dedicates it to Darwin.
585
They are mutual admirers to the point where, for example, Wallace is going to be a pallbearer at Darwin's funeral.
586
And in their day, this was referred to as the Darwin -Wallace theory.
587
It's only later that biologists and historians just started kind of forgetting about Wallace and crediting Darwin.
588
Now, there might be reasons for that.
589
Darwin came from a wealthy family.
590
The University of Cambridge did a great job at sort of amassing Darwin's collections and Darwin's writings.
591
And so we just have a better historical record of everything that Darwin did.
592
But at the time, it was the Darwin -Wallace theory.
593
And I think by today's scientific standards, given the genesis of this theory, the theory certainly of natural selection by the two individuals, we would be crediting both of them.
594
And it's just, you know, it's just the unfortunate sort of,
595
you know, accidents of time that people kept talking about Darwin and Wallace sort of faded to the background.
596
But I really feel in the last 25 years or so
597
that Wallace has seen sort of a renaissance and that people are much more aware of Wallace's huge contributions.
598
And then Wallace outlived Darwin by 30 years.
599
So he was a really important figure in the discussion of evolution because, you know, this was a brand new science.
600
It had relatively few advocates at the beginning, certainly people that really understood it well.
601
And so Wallace played a a huge role in getting people to help understand these ideas.
602
I think if Darwin and Wallace were alive today,
603
they would be so overjoyed by the detail with which we understand the process that they first figured out.
604
They knew variation was important.
605
They knew variation was the fuel of the evolutionary process, had no idea how that variation arose.
606
Now, any biologist can point right to the DNA in a newly hatched creature and say, there's the mutation.
607
That's what's going to make the difference.
608
So our understanding of the material basis of evolution is phenomenally strong.
609
And I think that would be extremely gratifying to them.
610
But these other manifestations, the role it plays in health and disease were nowhere in Darwin and Wallace's minds.
611
So I think that would,
612
again, further astound them that this process they figured out had such widespread ramifications beyond just the natural world.
613
What we've seen are striking parallels in how life evolves, how our immune system works,
614
and even how cancer arises this process of mutation and selection, this staircase.
615
So really the process that Darwin and Wallace had that first insight into is a universal process.
616
Wherever there's variation, wherever there's competition, selection will operate.
617
For me personally, as an evolutionary biologist,
618
this just underscores the explanatory power of evolutionary theory and the importance of understanding the evolutionary process.
619
You might think, well, the evolutionary process, let's just leave it to the scientists to worry about it.
620
But I think in our daily lives, you understand that this is why we vaccinate.
621
This is why we are now developing these strategies against cancer that we, of course, hope everybody will be able to benefit from.
622
That's a long way from the Beagle voyage of 160 years ago.
623
But that's fundamentally where Darwin and Wallace have brought us.
ऐप डाउनलोड करें
धाराप्रवाह बोलने के लिए ज़रूरी सब कुछ
AI उच्चारण स्कोरहर वाक्य का स्कोर
IPA अभ्यासहर ध्वनि में महारत
शब्दावलीअपना शब्द भंडार बनाएँ
शब्द गेमखेलते हुए सीखें
उसी चैनल से
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इस पाठ की शब्दावली और बोलने के सुझाव
यह स्पीकिंग पाठ वीडियो “How evolution works, in 54 minutes” पर आधारित है। सबसे ज़्यादा दोहराए गए शब्द ये हैं: mutation, cell, cancer, Darwin, process। इस वीडियो में शैडोइंग के लिए 455 वाक्य और 8516 शब्द हैं। बोला गया हिस्सा 54:32 लंबा है। वक्ता लगभग 156 शब्द प्रति मिनट की स्वाभाविक गति से बोलता है, जो रोज़मर्रा की बातचीत के करीब है। 82% शब्द अंग्रेज़ी के 3,000 सबसे आम शब्दों में से हैं; बाकी शब्द अभ्यास से पहले देख लेना अच्छा रहेगा।
इस वीडियो की मुख्य शब्दावली
वीडियो के 15 सीखने लायक शब्द, उच्चारण और अर्थ के साथ:
| शब्द | उच्चारण | अर्थ |
|---|---|---|
| gene संज्ञा | /d͡ʒiːn/ | जीन, वंशाणु |
| evolution संज्ञा | /ˌiːvəˈluːʃ(ə)n/ | क्रमविकास |
| staircase संज्ञा | /ˈstɛɹˌkeɪs/ | सीढ़ी, सोपान |
| evolutionary विशेषण | /ˌiː.vəˈluː.ʃən.ɛɹ.i/ | क्रमविकासीय |
| fossil संज्ञा | /ˈfɑsl̩/ | जीवाश्म |
| tumor संज्ञा | /tuː.məɹ/ | फुलाव, नववर्धन |
| arise क्रिया | /əˈɹaɪz/ | उद्गम |
| genetic विशेषण | /d͡ʒəˈnɛt.ɪk/ | अनुवांशिक |
| voyage संज्ञा | /ˈvɔɪ.ɪd͡ʒ/ | यात्रा |
| virus संज्ञा | /ˈvaɪ.ɹəs/ | विषाणु, वाइरस |
| distinct विशेषण | /dɪˈstɪŋkt/ | भिन्न |
| mechanism संज्ञा | /ˈmɛk.ə.nɪ.zəm/ | तंत्र, यंत्रावली |
| encounter क्रिया | /ɪnˈkaʊntɚ/ | सामना, भेंट |
| occur क्रिया | /əˈkɜː/ | बीतना |
| principle संज्ञा | /ˈpɹɪn.sɪ.pəl/ | जड़सूत्र, असूल |
वीडियो में आने वाली फ़्रेज़ल वर्ब
| शब्द | अर्थ |
|---|---|
| pick up क्रिया | उठाना |
| come back क्रिया | वापस आना |
| sort out क्रिया | ठीक करना |
दोहराने लायक वाक्य
वीडियो के छोटे, पूरे वाक्य जिन्हें आप रोज़ की बातचीत में इस्तेमाल कर सकते हैं:
- To the rest of us, it's instantly fatal.
- You know, do we have every brick?
- Do we have every intermediate?
- We've gotta fend these off.
- How do we find them?
इस वीडियो का व्याकरण
वक्ता जिन संरचनाओं का सबसे अधिक प्रयोग करता है, वीडियो के असली शब्दों के साथ:
| संरचना | वीडियो में |
|---|---|
| Present perfect continuous have/has been + -ing — पहले शुरू हुआ काम जो अब भी जारी है | we've been trying · we've been discussing |
| शर्त वाले वाक्य if + उपवाक्य, will/would + क्रिया — शर्त और उसका नतीजा | if mutation didn't happen all things would be · if my theory is true, this would be |
| Present perfect have/has + past participle — बीता हुआ काम जिसका असर अभी भी है | has happened · have come · they've done |
| Passive voice be + past participle — ज़ोर इस पर कि क्या होता है, न कि कौन करता है | was referred · be added · been estimated |
ध्यान देने योग्य उच्चारण
वक्ता 131 बार संक्षिप्त रूपों का प्रयोग करता है, जैसे they're, don't, we're। इन्हें वैसे ही छोटा बोलें जैसा आप सुनते हैं।
- “th” की ध्वनियाँ: hypothesis /haɪˈpɒθɪsɪs/, pathogen /ˈpæθəd͡ʒn̩/, sloth /slɔθ/
- “sh” और “zh” की ध्वनियाँ: mutation /mjuˈteɪʃən/, evolution /ˌiːvəˈluːʃ(ə)n/, evolutionary /ˌiː.vəˈluː.ʃən.ɛɹ.i/, variation /ˌvɛəɹiˈeɪʃn̩/, essentially /ɪˈsɛnʃəli/
- लंबे शब्द — बलाघात सही रखें: evolution /ˌiːvəˈluːʃ(ə)n/, evolutionary /ˌiː.vəˈluː.ʃən.ɛɹ.i/, essentially /ɪˈsɛnʃəli/, mechanism /ˈmɛk.ə.nɪ.zəm/, immunity /ɪˈmjuːnəti/
हिंदी भाषियों के लिए मुश्किल ध्वनियाँ:
- /v/ और /w/ का फ़र्क़ — /v/ में ऊपर के दाँत निचले होंठ को छूते हैं, /w/ में होंठ गोल होते हैं: evolution /ˌiːvəˈluːʃ(ə)n/, evolutionary /ˌiː.vəˈluː.ʃən.ɛɹ.i/, variation /ˌvɛəɹiˈeɪʃn̩/, evolve /ɪˈvɑlv/, voyage /ˈvɔɪ.ɪd͡ʒ/
- /z/ — इसे “ज” (/dʒ/) न बनाएँ: arise /əˈɹaɪz/, mechanism /ˈmɛk.ə.nɪ.zəm/, combinations /kɑmbɪˈneɪʃənz/, whereas /(h)wɛɹˈæz/, stairs /ˈstɛɹz/
- शब्द की शुरुआत में s + व्यंजन — पहले “इ” न जोड़ें: staircase /ˈstɛɹˌkeɪs/, specimen /ˈspɛsɪmɪn/, slight /slaɪt/, stairs /ˈstɛɹz/, slice /slaɪs/
इस वीडियो से अभ्यास कैसे करें
- पहले बिना बोले पूरा वीडियो एक बार सुनें और जो शब्द नहीं आते उन्हें लिख लें।
- 0.75× गति से शुरू करें, एक-एक वाक्य की शैडोइंग करें, और सहज लगने पर सामान्य गति पर लौटें।
- अपनी आवाज़ रिकॉर्ड करें और मूल से तुलना करें, ख़ासकर gene, evolution, staircase जैसे शब्दों पर ध्यान दें।
शैडोइंग तकनीक क्या है?
शैडोइंग (Shadowing) एक विज्ञान-समर्थित भाषा सीखने की तकनीक है जो मूल रूप से पेशेवर दुभाषिया प्रशिक्षण के लिए विकसित की गई थी। विधि सरल लेकिन शक्तिशाली है: आप मूल अंग्रेज़ी ऑडियो सुनते हैं और तुरंत इसे ज़ोर से दोहराते हैं — जैसे वक्ता की छाया 1-2 सेकंड की देरी से। शोध से पता चलता है कि यह उच्चारण सटीकता, स्वर, लय, जुड़ी हुई ध्वनियाँ, सुनने की समझ और बोलने की प्रवाहशीलता में काफ़ी सुधार करता है।