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The gene-centered view of evolution, gene selection theory, or selfish gene theory holds that adaptive evolution occurs through the differential survival of competing genes, increasing the frequency of those alleles whose phenotypic effects successfully promote their own propagation, with gene defined as "not just one single physical bit of DNA [but] all replicas of a particular bit of DNA distributed throughout the world".[1] The proponents of this viewpoint argue that, since heritable information is passed from generation to generation almost exclusively by genetic material, natural selection and evolution are best considered from the perspective of genes.
This is in contrast to the organism-centered viewpoint adopted historically by biologists. Proponents of the gene-centered viewpoint argue that it permits understanding of diverse phenomena such as altruism and intragenomic conflict that are otherwise difficult to explain from an organism-focused perspective.
The gene-centered view of evolution is a synthesis of the theory of evolution by natural selection, the particulate inheritance theory, and the non-transmission of acquired characters. It states that those alleles whose phenotypic effects successfully promote their own propagation will be favorably selected relative to their competitor alleles within the population. This process produces adaptations for the benefit of alleles that promote the reproductive success of the organism, or of other organisms containing the same allele (kin altruism and green-beard effects), or even its own propagation relative to the other genes within the same organism (intragenomic conflict).
The rejection of the inheritance of acquired characters, combined with the classical mathematical evolutionary biology developed by Ronald Fisher,[3] J. B. S. Haldane, and Sewall Wright, paved the way to the formulation of the selfish-gene theory.[clarification needed] For cases where environment can influence heredity, see epigenetics.[clarification needed]
According to Williams' 1966 book Adaptation and Natural Selection,
Williams argued that "[t]he natural selection of phenotypes cannot in itself produce cumulative change, because phenotypes are extremely temporary manifestations." Each phenotype is the unique product of the interaction between genome and environment. It does not matter how fit and fertile a phenotype is, it will eventually be destroyed and will never be duplicated.
Since 1954, it has been known that DNA is the main physical substrate to genetic information, and it is capable of high-fidelity replication through many generations. So, a particular sequence of DNA can have a high permanence and a low rate of endogenous change.
In normal sexual reproduction, an entire genome is the unique combination of father's and mother's chromosomes produced at the moment of fertilization. It is generally destroyed with its organism, because "meiosis and recombination destroy genotypes as surely as death."[8] Only half of it is transmitted to each descendant due to independent segregation.
The gene as an informational entity persists for an evolutionarily significant span of time through a lineage of many physical copies.
In his book River out of Eden, Dawkins coins the phrase God's utility function to explain his view on genes as units of selection. He uses this phrase as a synonym of the "meaning of life" or the "purpose of life". By rephrasing the word purpose in terms of what economists call a utility function, meaning "that which is maximized", Dawkins attempts to reverse-engineer the purpose in the mind of the Divine Engineer of Nature, or the Utility Function of God. Finally, Dawkins argues that it is a mistake to assume that an ecosystem or a species as a whole exists for a purpose. He writes that it is incorrect to suppose that individual organisms lead a meaningful life either; in nature, only genes have a utility function – to perpetuate their own existence with indifference to great sufferings inflicted upon the organisms they build, exploit and discard.
The phenotypic effect of a particular gene is contingent on its environment, including the fellow genes constituting with it the total genome. A gene never has a fixed effect, so how is it possible to speak of a gene for long legs? It is because of the phenotypic differences between alleles. One may say that one allele, all other things being equal or varying within certain limits, causes greater legs than its alternative. This difference enables the scrutiny of natural selection.
"A gene can have multiple phenotypic effects, each of which may be of positive, negative or neutral value. It is the net selective value of a gene's phenotypic effect that determines the fate of the gene."[12] For instance, a gene can cause its bearer to have greater reproductive success at a young age, but also cause a greater likelihood of death at a later age. If the benefit outweighs the harm, averaged out over the individuals and environments in which the gene happens to occur, then phenotypes containing the gene will generally be positively selected and thus the abundance of that gene in the population will increase.
Even so, it becomes necessary to model the genes in combination with their vehicle as well as in combination with the vehicle's environment.
The result is that "the prevalent genes in a sexual population must be those that, as a mean condition, through a large number of genotypes in a large number of situations, have had the most favourable phenotypic effects for their own replication."[13] In other words, we expect selfish genes ("selfish" meaning that it promotes its own survival without necessarily promoting the survival of the organism, group or even species). This theory implies that adaptations are the phenotypic effects of genes to maximize their representation in future generations. An adaptation is maintained by selection if it promotes genetic survival directly, or else some subordinate goal that ultimately contributes to successful reproduction.
The kin selection theory predicts that a gene may promote the recognition of kinship by historical continuity: a mammalian mother learns to identify her own offspring in the act of giving birth; a male preferentially directs resources to the offspring of mothers with whom he has copulated; the other chicks in a nest are siblings; and so on. The expected altruism between kin is calibrated by the value of p, also known as the coefficient of relatedness. For instance, an individual has a p = 1/2 in relation to his brother, and p = 1/8 to his cousin, so we would expect, ceteris paribus, greater altruism among brothers than among cousins. In this vein, geneticist J. B. S. Haldane famously joked, "Would I lay down my life to save my brother? No, but I would to save two brothers or eight cousins."[15] However, examining the human propensity for altruism, kin selection theory seems incapable of explaining cross-familiar, cross-racial and even cross-species acts of kindness.
Individuals opposing this gene-centric view include Ernst Mayr, Stephen Jay Gould, David Sloan Wilson, and philosopher Elliott Sober.
Proponents of multilevel selection (MLS) include E. O. Wilson, David Sloan Wilson, Elliott Sober, Richard E. Michod,[17] and Samir Okasha.[17]
Writing in the New York Review of Books, Gould has characterized the gene-centered perspective as confusing book-keeping with causality. Gould views selection as working on many levels, and has called attention to a hierarchical perspective of selection. Gould also called the claims of Selfish Gene "strict adaptationism", "ultra-Darwinism", and "Darwinian fundamentalism", describing them as excessively "reductionist". He saw the theory as leading to a simplistic "algorithmic" theory of evolution, or even to the re-introduction of a teleological principle.[18] Mayr went so far as to say "Dawkins' basic theory of the gene being the object of evolution is totally non-Darwinian."[19]
Gould also addressed the issue of selfish genes in his essay "Caring groups and selfish genes".[20] Gould acknowledged that Dawkins was not imputing conscious action to genes, but simply using a shorthand metaphor commonly found in evolutionary writings. To Gould, the fatal flaw was that "no matter how much power Dawkins wishes to assign to genes, there is one thing that he cannot give them – direct visibility to natural selection."[20] Rather, the unit of selection is the phenotype, not the genotype, because it is phenotypes that interact with the environment at the natural-selection interface. So, in Kim Sterelny's summation of Gould's view, "gene differences do not cause evolutionary changes in populations, they register those changes."[21] Richard Dawkins replied to this criticism in a later book, The Extended Phenotype, that Gould confused particulate genetics with particulate embryology, stating that genes do "blend", as far as their effects on developing phenotypes are concerned, but that they do not blend as they replicate and recombine down the generations.[10]
Since Gould's death in 2002, Niles Eldredge has continued with counter-arguments to gene-centered natural selection.[22] Eldredge notes that in Dawkins' book A Devil's Chaplain, which was published just before Eldredge's book, "Richard Dawkins comments on what he sees as the main difference between his position and that of the late Stephen Jay Gould. He concludes that it is his own vision that genes play a causal role in evolution," while Gould (and Eldredge) "sees genes as passive recorders of what worked better than what".[23]
This is in contrast to the organism-centered viewpoint adopted historically by biologists. Proponents of the gene-centered viewpoint argue that it permits understanding of diverse phenomena such as altruism and intragenomic conflict that are otherwise difficult to explain from an organism-focused perspective.
The gene-centered view of evolution is a synthesis of the theory of evolution by natural selection, the particulate inheritance theory, and the non-transmission of acquired characters. It states that those alleles whose phenotypic effects successfully promote their own propagation will be favorably selected relative to their competitor alleles within the population. This process produces adaptations for the benefit of alleles that promote the reproductive success of the organism, or of other organisms containing the same allele (kin altruism and green-beard effects), or even its own propagation relative to the other genes within the same organism (intragenomic conflict).
Overview
The gene-centered view of evolution is a different way of looking at the basis of evolutionary development. It turns the whole solution of evolution inside-out for the purpose of examination. What this new perspective reveals is a more easily understood model for the evolution of social characteristics such as selfishness and altruism that much of the study of evolution, caught up in the survival of the individual organisms, or, alternatively, groups of organisms, overlooks.Acquired characteristics are not genetically inherited
Discoveries in science such as the formulation of the central dogma of molecular biology made it clear that the inheritance of acquired characteristics (such as wealth) was not a genetic process and identified genes as lasting entities that survive through many generations. Maynard Smith summarized the issue:| “ | If the central dogma is true, and if it is also true that nucleic acids are the only means whereby information is transmitted between generations, this has crucial implications for evolution. It would imply that all evolutionary novelty requires changes in nucleic acids, and that these changes – mutations – are essentially accidental and non-adaptive in nature. Changes elsewhere – in the egg cytoplasm, in materials transmitted through the placenta, in the mother's milk – might alter the development of the child, but, unless the changes were in nucleic acids, they would have no long-term evolutionary effects. | ” |
The rejection of the inheritance of acquired characters, combined with the classical mathematical evolutionary biology developed by Ronald Fisher,[3] J. B. S. Haldane, and Sewall Wright, paved the way to the formulation of the selfish-gene theory.[clarification needed] For cases where environment can influence heredity, see epigenetics.[clarification needed]
The gene as the unit of selection
The view of the gene as the unit of selection was developed mainly in the works of W. D. Hamilton,[4][5][6] Colin Pittendrigh[7] and George C. Williams.[8] It was later popularized by Richard Dawkins in his books The Selfish Gene (1976)[9] and The Extended Phenotype (1982).[10]According to Williams' 1966 book Adaptation and Natural Selection,
| “ | [t]he essence of the genetical theory of natural selection is a statistical bias in the relative rates of survival of alternatives (genes, individuals, etc.). The effectiveness of such bias in producing adaptation is contingent on the maintenance of certain quantitative relationships among the operative factors. One necessary condition is that the selected entity must have a high degree of permanence and a low rate of endogenous change, relative to the degree of bias (differences in selection coefficients). | ” |
Williams argued that "[t]he natural selection of phenotypes cannot in itself produce cumulative change, because phenotypes are extremely temporary manifestations." Each phenotype is the unique product of the interaction between genome and environment. It does not matter how fit and fertile a phenotype is, it will eventually be destroyed and will never be duplicated.
Since 1954, it has been known that DNA is the main physical substrate to genetic information, and it is capable of high-fidelity replication through many generations. So, a particular sequence of DNA can have a high permanence and a low rate of endogenous change.
In normal sexual reproduction, an entire genome is the unique combination of father's and mother's chromosomes produced at the moment of fertilization. It is generally destroyed with its organism, because "meiosis and recombination destroy genotypes as surely as death."[8] Only half of it is transmitted to each descendant due to independent segregation.
The gene as an informational entity persists for an evolutionarily significant span of time through a lineage of many physical copies.
In his book River out of Eden, Dawkins coins the phrase God's utility function to explain his view on genes as units of selection. He uses this phrase as a synonym of the "meaning of life" or the "purpose of life". By rephrasing the word purpose in terms of what economists call a utility function, meaning "that which is maximized", Dawkins attempts to reverse-engineer the purpose in the mind of the Divine Engineer of Nature, or the Utility Function of God. Finally, Dawkins argues that it is a mistake to assume that an ecosystem or a species as a whole exists for a purpose. He writes that it is incorrect to suppose that individual organisms lead a meaningful life either; in nature, only genes have a utility function – to perpetuate their own existence with indifference to great sufferings inflicted upon the organisms they build, exploit and discard.
Organisms as vehicles
Genes are not naked in the world. They are usually packed together inside a genome, which is itself contained inside an organism. Genes group together into genomes because "genetic replication makes use of energy and substrates that are supplied by the metabolic economy in much greater quantities than would be possible without a genetic division of labour."[11] They build vehicles to promote their mutual interests of jumping into the next generation of vehicles. As Dawkins puts it, organisms are the "survival machines" of genes.[9]The phenotypic effect of a particular gene is contingent on its environment, including the fellow genes constituting with it the total genome. A gene never has a fixed effect, so how is it possible to speak of a gene for long legs? It is because of the phenotypic differences between alleles. One may say that one allele, all other things being equal or varying within certain limits, causes greater legs than its alternative. This difference enables the scrutiny of natural selection.
"A gene can have multiple phenotypic effects, each of which may be of positive, negative or neutral value. It is the net selective value of a gene's phenotypic effect that determines the fate of the gene."[12] For instance, a gene can cause its bearer to have greater reproductive success at a young age, but also cause a greater likelihood of death at a later age. If the benefit outweighs the harm, averaged out over the individuals and environments in which the gene happens to occur, then phenotypes containing the gene will generally be positively selected and thus the abundance of that gene in the population will increase.
Even so, it becomes necessary to model the genes in combination with their vehicle as well as in combination with the vehicle's environment.
Selfish-gene theory
The selfish-gene theory of natural selection can be restated as follows:[12]| “ | Genes do not present themselves naked to the scrutiny of natural selection, instead they present their phenotypic effects. [...] Differences in genes give rise to differences in these phenotypic effects. Natural selection acts on the phenotypic differences and thereby on genes. Thus genes come to be represented in successive generations in proportion to the selective value of their phenotypic effects. | ” |
The result is that "the prevalent genes in a sexual population must be those that, as a mean condition, through a large number of genotypes in a large number of situations, have had the most favourable phenotypic effects for their own replication."[13] In other words, we expect selfish genes ("selfish" meaning that it promotes its own survival without necessarily promoting the survival of the organism, group or even species). This theory implies that adaptations are the phenotypic effects of genes to maximize their representation in future generations. An adaptation is maintained by selection if it promotes genetic survival directly, or else some subordinate goal that ultimately contributes to successful reproduction.
Individual altruism and genetic egoism
The gene is a unit of hereditary information that exists in many physical copies in the world, and which particular physical copy will be replicated and originate new copies does not matter from the gene's point of view.[14] A selfish gene could be favored by selection by producing altruism among organisms containing it. The idea is summarized as follows:If a gene copy confers a benefit B on another vehicle at cost C to its own vehicle, its costly action is strategically beneficial if pB > C, where p is the probability that a copy of the gene is present in the vehicle that benefits. Actions with substantial costs therefore require significant values of p. Two kinds of factors ensure high values of p: relatedness (kinship) and recognition (green beards).A gene in a somatic cell of an individual may forego replication to promote the transmission of its copies in the germ line cells. It ensures the high value of p = 1 due to their constant contact and their common origin from the zygote.
—Haig,[11] 1997, p. 288
The kin selection theory predicts that a gene may promote the recognition of kinship by historical continuity: a mammalian mother learns to identify her own offspring in the act of giving birth; a male preferentially directs resources to the offspring of mothers with whom he has copulated; the other chicks in a nest are siblings; and so on. The expected altruism between kin is calibrated by the value of p, also known as the coefficient of relatedness. For instance, an individual has a p = 1/2 in relation to his brother, and p = 1/8 to his cousin, so we would expect, ceteris paribus, greater altruism among brothers than among cousins. In this vein, geneticist J. B. S. Haldane famously joked, "Would I lay down my life to save my brother? No, but I would to save two brothers or eight cousins."[15] However, examining the human propensity for altruism, kin selection theory seems incapable of explaining cross-familiar, cross-racial and even cross-species acts of kindness.
Green-beard effect
Green-beard effects gained their name from a thought-experiment of Richard Dawkins,[9] who considered the possibility of a gene that caused its possessors to develop a green beard and to be nice to other green-bearded individuals. Since then, "green-beard effect" has come to refer to forms of genetic self-recognition in which a gene in one individual might direct benefits to other individuals that possess the gene. Such genes are essentially especially selfish, benefiting themselves regardless of the fates of their vehicles.All kinds of altruism
Kindness
On the other hand, a single trait, group reciprocal kindness, is capable of explaining the vast majority of altruism that is generally accepted as "good" by modern societies. Imagine a green-bearding behavioral trait whose recognition does not depend on the recognition of some external feature such as beard color, but relies on recognition of the behavior itself. Imagine now that the behavior is altruistic. The success of such a trait in sufficiently intelligent and undeceived organisms is implicit. Moreover, the existence of such a trait predicts a tendency for kindness to unrelated organisms that are apparently kind, even if the organisms are of a completely different species. Moreover, the gene need not be exactly the same, so long as the effect is similar. Multiple versions of the gene—or even meme—would have virtually the same effect in a sort of symbiotic green-bearding cycle of altruism.Deceit
Whenever recognition plays a role in evolution, so does deception. Just like the harmless lizard that has evolved a pattern that mimics its poisonous cousin and therefore tricks predators, the selfish creature may pretend to be kind by "growing a green beard" (whatever that green beard may be). Thus green-bearding and the selfish-gene theory also give rise to an explanation for the evolution of lies and deceit, characteristics that do not benefit the population as a whole.Intragenomic conflict
As genes are capable of producing individual altruism, they are capable of producing conflict among genes inside the genome of one individual. This phenomenon is called intragenomic conflict and arises when one gene promotes its own replication in detriment to other genes in the genome. The classic example is segregation distorter genes that cheat during meiosis or gametogenesis and end up in more than half of the functional gametes. These genes persist even resulting in reduced fertility. Egbert Leigh compared the genome to "a parliament of genes: each acts in its own self-interest, but if its acts hurt the others, they will combine together to suppress it" to explain the relative low occurrence of intragenomic conflict.[16]Price equation
The Price equation (also known as Price's equation) is a covariance equation that is a mathematical description of evolution and natural selection. The Price equation was derived by George R. Price, working in London to rederive W. D. Hamilton's work on kin selection.Main figures in selection debate
Besides Richard Dawkins and George C. Williams, other biologists and philosophers have expanded and refined the selfish-gene theory, such as John Maynard Smith, George R. Price, Robert Trivers, David Haig, Helena Cronin, David Hull, Philip Kitcher, and Daniel C. Dennett.Individuals opposing this gene-centric view include Ernst Mayr, Stephen Jay Gould, David Sloan Wilson, and philosopher Elliott Sober.
Proponents of multilevel selection (MLS) include E. O. Wilson, David Sloan Wilson, Elliott Sober, Richard E. Michod,[17] and Samir Okasha.[17]
Criticisms
Prominent opponents of this gene-centric view of evolution include evolutionary biologist Ernst Mayr, paleontologist Stephen Jay Gould, biologist and anthropologist David Sloan Wilson, and philosopher Elliott Sober.Writing in the New York Review of Books, Gould has characterized the gene-centered perspective as confusing book-keeping with causality. Gould views selection as working on many levels, and has called attention to a hierarchical perspective of selection. Gould also called the claims of Selfish Gene "strict adaptationism", "ultra-Darwinism", and "Darwinian fundamentalism", describing them as excessively "reductionist". He saw the theory as leading to a simplistic "algorithmic" theory of evolution, or even to the re-introduction of a teleological principle.[18] Mayr went so far as to say "Dawkins' basic theory of the gene being the object of evolution is totally non-Darwinian."[19]
Gould also addressed the issue of selfish genes in his essay "Caring groups and selfish genes".[20] Gould acknowledged that Dawkins was not imputing conscious action to genes, but simply using a shorthand metaphor commonly found in evolutionary writings. To Gould, the fatal flaw was that "no matter how much power Dawkins wishes to assign to genes, there is one thing that he cannot give them – direct visibility to natural selection."[20] Rather, the unit of selection is the phenotype, not the genotype, because it is phenotypes that interact with the environment at the natural-selection interface. So, in Kim Sterelny's summation of Gould's view, "gene differences do not cause evolutionary changes in populations, they register those changes."[21] Richard Dawkins replied to this criticism in a later book, The Extended Phenotype, that Gould confused particulate genetics with particulate embryology, stating that genes do "blend", as far as their effects on developing phenotypes are concerned, but that they do not blend as they replicate and recombine down the generations.[10]
Since Gould's death in 2002, Niles Eldredge has continued with counter-arguments to gene-centered natural selection.[22] Eldredge notes that in Dawkins' book A Devil's Chaplain, which was published just before Eldredge's book, "Richard Dawkins comments on what he sees as the main difference between his position and that of the late Stephen Jay Gould. He concludes that it is his own vision that genes play a causal role in evolution," while Gould (and Eldredge) "sees genes as passive recorders of what worked better than what".[23]
