So the second video isn't as interesting as most of the other ones on here, so I will kind of mash it up with the first one a little bit with a different focus. (I watched all of them before writing the first post.)
I am not familiar with this particular study but it is a common one. The classic example is the famous peppered moth study which has come under a lot of fire in recent years for its methodology, but the basic principle is sound. (For instance, it came out that the pictures of moths resting on trees were actually dead moths pinned there by the photographer, and not live moths behaving normally as the study implied.) Basically they studied several populations of mice, some which live on desert sand and others which live on lava flows that are a thousand years old. They found that the populations which lived on the lava flows had mostly dark fur and the ones living on sandier terrain had light fur. This is consistent with the Darwinian explanation: It's a lot easier for predators to see mice that stand out against their background, and such mice will be selected out of the population over time versus mice with more convenient pigmentation. The basic premise of the video is correct: This does appear to be a powerful demonstration of the Darwinian mechanism of random mutation and natural selection. The latter half of the video voyages into an idea called "convergent evolution", a term never actually used in the video, but that's clearly what they are talking about. I can only assume it isn't so named because it remains something of a controversial idea. There is also a revealing segment where Dr. Carroll passionately denies the contention that the Darwinian mechanism is a purely random process, and calls this a "misconception". Well, he's right. It is a misconception. Before I dig into the science, I want to relate a bit of the history behind some of the ideas in this video relating to the randomness of evolution and convergent evolution.
This misconception about evolution has become and remained so widespread because evolutionary biologists and other evangelists for Darwin's theory have consistently and very publicly emphasized its random nature because it undermines religious faith. Evolution, they say, is distinguishable from any sort of creation by God because a creator makes things for a purpose and evolution doesn't. Therefore random, purposeless, unguided, evolution removes God as creator and furthermore, because there are all sorts of purposeless things in nature, so they say, this is evidence against the existence of God, or at least against evidence for creation. So when Dr. Carroll insists that evolution is not random, the informed viewer should sense a tension with the way evolutionary evangelists, Dr. Carroll's forebears, have gone about misleading the public about their own theory for the better part of the last century. Better, the informed viewer should wonder why contemporary evangelists, oh I'm sorry, evolutionists are abandoning their favorite weapon against religion. I would suggest to such a person that the arguments which treat evolution according to the rules of random probability advanced by intelligent design theorists have struck home, and that's another reason why these videos put a big smile on my face. It's evidence that we are driving the debate now, even winning it.
If evolution is driven by mostly random processes then we should expect that populations of organisms facing the same challenge will not find the same adaptation suited to the same problem. A random search of a very large range of possibilities makes finding the same solution to the same problem more than once extremely unlikely. Historically evolutionists have almost universally believed in both the random factor as a driving force as well as a nearly unlimited range of possible adaptations and consequently have been quite hostile to the idea of "convergent evolution". Convergent evolution is just the opposite idea: that evolution will routinely find the same solution to the same problem, either because solutions are few and far between or the process is not as random as advertised, or both. The most well-known proponent of convergent evolution is Simon Conway Morris, a paleontologist well known for his work on the Burgess shale fossil bed. Due to the efforts of scientists like Morris, convergent evolution has slowly moved from the lunatic fringe of evolutionary theory to the somewhat respectable mainstream over the last thirty years or so, though it remains controversial. Dr. Carroll here comes out clearly in favor of convergent evolution, though he declines to use the term. So if he seems a bit like an evangelist in these videos, understand that he is not only preaching to creationists; he is also preaching to his fellow evolutionists. Yes, dear viewers, evolutionists disagree with each other over their own theory, reason enough to wonder if the science is really settled. At the very least raising the issue with the average evolution believer and watching them chase their tails for awhile might relieve the monotony of your day. It's probably not all I'm cracking it up to be, but it's at least mildly amusing.
Now to the science. I'll get straight to the point. The biologist in the video who studies the mice, Michael Nachman, explains that the difference between light and dark mice can be explained by four mutations in the gene called MC1R. He believes that since the lava flows are a thousand years old, this dark mutation must also be a thousand years old and the light-colored mice are the wild-type. This assumption is glossed over in the video, but there is nothing to suggest that is the case. In fact, it is much more likely that the dark fur version, or allele, of MC1R is the original and the light-colored allele is the mutation. Why? As any two year-old knows, or anyone observing a two-year-old, it's much easier to break something than build something. Let me explain what I mean.
Wikipedia: "Alleles for constitutively active MC1R are inherited dominantly and result in a black coat colour, whereas alleles for dysfunctional MC1R are recessive and result in a light coat colour." [Emphasis added]
The difference between these two alleles is not the difference between a happy mutation that changed a working genetic mechanism from making a dark color to making a white color. The difference is between a working allele and a broken allele. This is usually what is happening genetically when we're talking about light and dark colors, including in human hair for example. Going back to the first video, this is relevant to the discussion about genetic "switches" that turn on and off as well as basic Mendelian genetics involving dominant and recessive alleles. If you took high school biology and wondered why dominant alleles only require one copy to express their trait while recessive genes require two copies, wonder no more. Dominant alleles are dominant because they work. Even with only one copy, the organism will still express the trait because it has at least one working gene and can produce the corresponding protein product(s). The recessive trait is only expressed when both copies are broken and the organism cannot make any.
A broken gene could have the opposite effect, however, because of complicated genetic mechanisms. For instance, a broken or recessive gene could cause a particular working genetic mechanism to be expressed, or expressed more, by failure to express a working inhibitor. This is quite common. A gene that would otherwise work is bound by an inhibitor protein or RNA, which prevents it from being produced. But if the inhibitor protein or RNA is broken such that it no longer binds its target, then the target can be produced and the organism will express a positive trait that it did not express before. In this way mutations that break genes can potentially explain any evolutionary adaptation, which is why one should always inquire as to the actual genetic and molecular mechanisms involved before getting wide-eyed about the power of Darwinian evolution. Does the Darwinian mechanism of random mutation and natural selection work? Yes. Does it make novel, functional genes? Almost never. (You'll have to wait for the anti-freeze proteins in the third video for a notable exception.)
In the case of MC1R, the light-colored allele is the broken, recessive gene and the dark-colored allele is the working version, producing a pigment called eumelanin. But why do I say this is evidence that the dark-colored version came first, contra Nachmann? What if light-colored mice really did come first and evolved a mechanism that made the dark pigment?
First of all, this was not observed in the study. That's important to remember. Nobody cataloged the genes of all of these mice populations over the last thousand years and suddenly observed a brand new mutation making a dark pigment that was never there before. The idea that the dark allele came later is an assumption. There's no reason why the mice could not have broken their genes to adapt to light-colored sand while a small portion of the population retained the original dark allele. When the lava flow formed, some of these mice with the original working gene began to breed preferentially and the population changed back to the original color. We don't know if that's what happened, but we also don't know if the story presented in the video is true either.
More importantly, it's intuitively obvious that breaking a precision machine like a protein or RNA is much easier than building one. But don't take my word for it. Here's the textbook from my college genetics class:
Gain-of-function mutations
Because mutations events introduce random genetic changes, most of the time they result in loss of function. The mutation events are like bullets being fired at a complex machine; most of the time they will inactivate it. However, it is conceivable that in rare cases a bullet will strike the machine in such a way that it produces some new function. So it is with mutation events; sometimes the random change by pure chance confers some new function on the gene. In a heterozygote, the new function will be expressed, and therefore the gain-of-function mutation most likely will act like a dominant allele and produce some kind of new phenotype. Gain of function is represented in Figure 15-12c. [1]
The figure referred to is a schematic diagram showing how a gain-of-function mutation would conceivably work if they actually found one, not a compilation of the scientific evidence for something that "is conceivable" "in rare cases" that "some new function" might be produced in one's imagination. But I think the metaphor of firing a bullet into a complex machine, such as a car or computer, is quite apt and refreshingly honest. Random mutations are almost invariably destructive. When they are not destructive, they are neutral. When they increase fitness, they do so by destroying a previously working function and the organism happens to gain something by doing so. In the case of the rock pocket mice, they gain some camouflage by destroying their dark fur pigment. Then the situation changed, and they needed to breed with a member of the same species carrying the original gene in order to get the trait back. Absent any special evidence, we should assume that the working MC1R is the original and the light-colored, broken version is the mutation.
But what does all this have to do with convergent evolution? Traditionally evolutionists have assumed that variation is virtually unlimited. But convergent evolution suggests that it is not. Convergent evolution admits that solutions to problems are rare, and so if an organism adapts at all it will likely find the same or similar solution to what other populations have found. I find the metaphor of switches in the stickleback video to be quite helpful. Genes do not continuously evolve in one direction, slowly increasing fitness over vast periods of time. Rather, they either work or they get broken and don't work. They are either switched on or off, and this suggests a fundamental limit to the amount of variability a population can accommodate. It suggests just what convergent evolution does: that solutions to problems are few and limited to what can be accomplished by turning genes on or off, because the only thing that random mutations do in practice is destroy a working gene in part of a population.
Suppose a species starts out with all working genes. Then a random mutation breaks a particular gene the species doesn't need or even benefits by losing, and this mutation spreads throughout the population. Suppose that a population in another location actually needs the working gene, and so any mutations which break that gene are selected out. Over time, each population will evolve into its own niche because of natural selection. Perhaps they interbreed enough that the population which lost the functional gene might regain it through breeding with the one that retained it, and in so doing switch the gene back on. But it won't go any further, and it can never break genes that are essential to its survival. Many combinations of broken and working genes are possible, but the number of combinations and the variations available are limited, so the species as a whole stays within these limits and never evolves outside them. That is the real picture of evolution that the observable, scientific evidence supports.
Now that's whack.
1. "An Introduction to Genetic Analysis" Seventh Edition, published by W.H. Freeman, New York, pp. 472.
NOTE: Richard Lewontin co-authoried this textbook, the same guy who kindly explained that the purpose of his particular cadre of scientists was to eliminate God from science because, and I quote, "we cannot allow a divine foot in the door".
I am not familiar with this particular study but it is a common one. The classic example is the famous peppered moth study which has come under a lot of fire in recent years for its methodology, but the basic principle is sound. (For instance, it came out that the pictures of moths resting on trees were actually dead moths pinned there by the photographer, and not live moths behaving normally as the study implied.) Basically they studied several populations of mice, some which live on desert sand and others which live on lava flows that are a thousand years old. They found that the populations which lived on the lava flows had mostly dark fur and the ones living on sandier terrain had light fur. This is consistent with the Darwinian explanation: It's a lot easier for predators to see mice that stand out against their background, and such mice will be selected out of the population over time versus mice with more convenient pigmentation. The basic premise of the video is correct: This does appear to be a powerful demonstration of the Darwinian mechanism of random mutation and natural selection. The latter half of the video voyages into an idea called "convergent evolution", a term never actually used in the video, but that's clearly what they are talking about. I can only assume it isn't so named because it remains something of a controversial idea. There is also a revealing segment where Dr. Carroll passionately denies the contention that the Darwinian mechanism is a purely random process, and calls this a "misconception". Well, he's right. It is a misconception. Before I dig into the science, I want to relate a bit of the history behind some of the ideas in this video relating to the randomness of evolution and convergent evolution.
This misconception about evolution has become and remained so widespread because evolutionary biologists and other evangelists for Darwin's theory have consistently and very publicly emphasized its random nature because it undermines religious faith. Evolution, they say, is distinguishable from any sort of creation by God because a creator makes things for a purpose and evolution doesn't. Therefore random, purposeless, unguided, evolution removes God as creator and furthermore, because there are all sorts of purposeless things in nature, so they say, this is evidence against the existence of God, or at least against evidence for creation. So when Dr. Carroll insists that evolution is not random, the informed viewer should sense a tension with the way evolutionary evangelists, Dr. Carroll's forebears, have gone about misleading the public about their own theory for the better part of the last century. Better, the informed viewer should wonder why contemporary evangelists, oh I'm sorry, evolutionists are abandoning their favorite weapon against religion. I would suggest to such a person that the arguments which treat evolution according to the rules of random probability advanced by intelligent design theorists have struck home, and that's another reason why these videos put a big smile on my face. It's evidence that we are driving the debate now, even winning it.
If evolution is driven by mostly random processes then we should expect that populations of organisms facing the same challenge will not find the same adaptation suited to the same problem. A random search of a very large range of possibilities makes finding the same solution to the same problem more than once extremely unlikely. Historically evolutionists have almost universally believed in both the random factor as a driving force as well as a nearly unlimited range of possible adaptations and consequently have been quite hostile to the idea of "convergent evolution". Convergent evolution is just the opposite idea: that evolution will routinely find the same solution to the same problem, either because solutions are few and far between or the process is not as random as advertised, or both. The most well-known proponent of convergent evolution is Simon Conway Morris, a paleontologist well known for his work on the Burgess shale fossil bed. Due to the efforts of scientists like Morris, convergent evolution has slowly moved from the lunatic fringe of evolutionary theory to the somewhat respectable mainstream over the last thirty years or so, though it remains controversial. Dr. Carroll here comes out clearly in favor of convergent evolution, though he declines to use the term. So if he seems a bit like an evangelist in these videos, understand that he is not only preaching to creationists; he is also preaching to his fellow evolutionists. Yes, dear viewers, evolutionists disagree with each other over their own theory, reason enough to wonder if the science is really settled. At the very least raising the issue with the average evolution believer and watching them chase their tails for awhile might relieve the monotony of your day. It's probably not all I'm cracking it up to be, but it's at least mildly amusing.
Now to the science. I'll get straight to the point. The biologist in the video who studies the mice, Michael Nachman, explains that the difference between light and dark mice can be explained by four mutations in the gene called MC1R. He believes that since the lava flows are a thousand years old, this dark mutation must also be a thousand years old and the light-colored mice are the wild-type. This assumption is glossed over in the video, but there is nothing to suggest that is the case. In fact, it is much more likely that the dark fur version, or allele, of MC1R is the original and the light-colored allele is the mutation. Why? As any two year-old knows, or anyone observing a two-year-old, it's much easier to break something than build something. Let me explain what I mean.
Wikipedia: "Alleles for constitutively active MC1R are inherited dominantly and result in a black coat colour, whereas alleles for dysfunctional MC1R are recessive and result in a light coat colour." [Emphasis added]
The difference between these two alleles is not the difference between a happy mutation that changed a working genetic mechanism from making a dark color to making a white color. The difference is between a working allele and a broken allele. This is usually what is happening genetically when we're talking about light and dark colors, including in human hair for example. Going back to the first video, this is relevant to the discussion about genetic "switches" that turn on and off as well as basic Mendelian genetics involving dominant and recessive alleles. If you took high school biology and wondered why dominant alleles only require one copy to express their trait while recessive genes require two copies, wonder no more. Dominant alleles are dominant because they work. Even with only one copy, the organism will still express the trait because it has at least one working gene and can produce the corresponding protein product(s). The recessive trait is only expressed when both copies are broken and the organism cannot make any.
A broken gene could have the opposite effect, however, because of complicated genetic mechanisms. For instance, a broken or recessive gene could cause a particular working genetic mechanism to be expressed, or expressed more, by failure to express a working inhibitor. This is quite common. A gene that would otherwise work is bound by an inhibitor protein or RNA, which prevents it from being produced. But if the inhibitor protein or RNA is broken such that it no longer binds its target, then the target can be produced and the organism will express a positive trait that it did not express before. In this way mutations that break genes can potentially explain any evolutionary adaptation, which is why one should always inquire as to the actual genetic and molecular mechanisms involved before getting wide-eyed about the power of Darwinian evolution. Does the Darwinian mechanism of random mutation and natural selection work? Yes. Does it make novel, functional genes? Almost never. (You'll have to wait for the anti-freeze proteins in the third video for a notable exception.)
In the case of MC1R, the light-colored allele is the broken, recessive gene and the dark-colored allele is the working version, producing a pigment called eumelanin. But why do I say this is evidence that the dark-colored version came first, contra Nachmann? What if light-colored mice really did come first and evolved a mechanism that made the dark pigment?
First of all, this was not observed in the study. That's important to remember. Nobody cataloged the genes of all of these mice populations over the last thousand years and suddenly observed a brand new mutation making a dark pigment that was never there before. The idea that the dark allele came later is an assumption. There's no reason why the mice could not have broken their genes to adapt to light-colored sand while a small portion of the population retained the original dark allele. When the lava flow formed, some of these mice with the original working gene began to breed preferentially and the population changed back to the original color. We don't know if that's what happened, but we also don't know if the story presented in the video is true either.
More importantly, it's intuitively obvious that breaking a precision machine like a protein or RNA is much easier than building one. But don't take my word for it. Here's the textbook from my college genetics class:
Gain-of-function mutations
Because mutations events introduce random genetic changes, most of the time they result in loss of function. The mutation events are like bullets being fired at a complex machine; most of the time they will inactivate it. However, it is conceivable that in rare cases a bullet will strike the machine in such a way that it produces some new function. So it is with mutation events; sometimes the random change by pure chance confers some new function on the gene. In a heterozygote, the new function will be expressed, and therefore the gain-of-function mutation most likely will act like a dominant allele and produce some kind of new phenotype. Gain of function is represented in Figure 15-12c. [1]
The figure referred to is a schematic diagram showing how a gain-of-function mutation would conceivably work if they actually found one, not a compilation of the scientific evidence for something that "is conceivable" "in rare cases" that "some new function" might be produced in one's imagination. But I think the metaphor of firing a bullet into a complex machine, such as a car or computer, is quite apt and refreshingly honest. Random mutations are almost invariably destructive. When they are not destructive, they are neutral. When they increase fitness, they do so by destroying a previously working function and the organism happens to gain something by doing so. In the case of the rock pocket mice, they gain some camouflage by destroying their dark fur pigment. Then the situation changed, and they needed to breed with a member of the same species carrying the original gene in order to get the trait back. Absent any special evidence, we should assume that the working MC1R is the original and the light-colored, broken version is the mutation.
But what does all this have to do with convergent evolution? Traditionally evolutionists have assumed that variation is virtually unlimited. But convergent evolution suggests that it is not. Convergent evolution admits that solutions to problems are rare, and so if an organism adapts at all it will likely find the same or similar solution to what other populations have found. I find the metaphor of switches in the stickleback video to be quite helpful. Genes do not continuously evolve in one direction, slowly increasing fitness over vast periods of time. Rather, they either work or they get broken and don't work. They are either switched on or off, and this suggests a fundamental limit to the amount of variability a population can accommodate. It suggests just what convergent evolution does: that solutions to problems are few and limited to what can be accomplished by turning genes on or off, because the only thing that random mutations do in practice is destroy a working gene in part of a population.
Suppose a species starts out with all working genes. Then a random mutation breaks a particular gene the species doesn't need or even benefits by losing, and this mutation spreads throughout the population. Suppose that a population in another location actually needs the working gene, and so any mutations which break that gene are selected out. Over time, each population will evolve into its own niche because of natural selection. Perhaps they interbreed enough that the population which lost the functional gene might regain it through breeding with the one that retained it, and in so doing switch the gene back on. But it won't go any further, and it can never break genes that are essential to its survival. Many combinations of broken and working genes are possible, but the number of combinations and the variations available are limited, so the species as a whole stays within these limits and never evolves outside them. That is the real picture of evolution that the observable, scientific evidence supports.
Now that's whack.
1. "An Introduction to Genetic Analysis" Seventh Edition, published by W.H. Freeman, New York, pp. 472.
NOTE: Richard Lewontin co-authoried this textbook, the same guy who kindly explained that the purpose of his particular cadre of scientists was to eliminate God from science because, and I quote, "we cannot allow a divine foot in the door".
