Nov 03 2010
he gene-centered view of evolution (aka gene selection theory or selfish gene theory) holds that natural selection acts through the differential survival of competing genes, increasing the frequency of those alleles whose phenotypic effects successfully promote their own propagation. According to this theory, adaptations are the phenotypic result through which genes achieve their propagation.
The genetic “selfishness” here means maximizing its own transmission, not any other more emotionally or morally loaded meaning of the word selfishness. However the real manifesto of the gene-centered view of evolution is the somewhat self-deprecatory Central Dogma as advanced by Francis Crick (1916–2004), one of the discoverers of the molecular structure of DNA in 1958:
The central dogma of molecular biology deals with the detailed residue-by-residue transfer of sequential information. It states that information cannot be transferred back from protein to either protein or nucleic acid.
In other words, once information gets into protein, it can’t flow back to nucleic acid. This extreme view of genetic determinism has largely fallen by the wayside. Information jumps all around the genome, from genes to proteins to transcription factors and back to genes. In addition, the information contains in the DNA code is of rather low information density (you can specific any one nucleotide with as little as two ‘bits’ of information: 01, 11, 10, 00). Glycomic influences (attaching branching sugars to proteins) add immeasurably more information density and control much of the actual fate of the proteins coded by DNA.
Prior to Dawkins, the selfish gene concept was advanced by George C. Williams (1926-2010) in his 1966 work Adaptation and Natural Selection. In it, Williams argued that 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.
The natural selection of phenotypes cannot in itself produce cumulative change, because phenotypes are extremely temporary manifestations.
In essence, the selfish gene concept attempts to address the very basic problem whose identification goes back to August Weismann (1834-1914) —what are the levels at which natural selection works? In particular, how and why would natural selection further a trait that is good for the survival of a group or society, but injurious to the individual? An example is the alarm notes sounded by certain species of birds. Although good for the group, a single bird that sounds the alarm risks being identified and perhaps eaten by a predator. According to natural selection, these “altruistic” traits must have been selected because they benefit the group’s survival.
However, there are obvious shortcomings with this argument. For example, if a gene crops up that results in a bird becoming a “non-caller,” one might expect that this gene would spread in the population and replace the genes for altruistic behavior compared with the altruistic “callers” who would become less likely to survive and reproduce.
R.A. Fisher (1890-1962) and J.B.S Haldane (1892-1964) recognized this problem, but William D. Hamilton (1936-2000) provided an answer, in what became known as Hamilton’s Rule. In each behavior-evoking situation, the individual assesses his neighbors’ fitness against his own according to the coefficients of relationship appropriate to the situation. In other words, the beneficiaries of altruistic actions are almost always the members of the altruist’s family. Even if the altruist himself has less offspring, the genes underlying the altruist’s behavior increase in frequency.
The selfish gene concept has been codified (at least for the general public) in the work of Richard Dawkins, particularly in the appropriately titled The Selfish Gene (1976). Dawkins took up Hamilton’s approach and extended it to a “gene’s eye view.” According to Dawkins this selfish behavior can help us to understand the evolution of all adaptive traits. To Dawkins, the genes are “selfish” because they do not concern themselves with the reproductive success of the individual insomuch as they are interested in the propagation of the gene in subsequent generations.
To Dawkins, we are the “survival machines” of our genes. Key to the concept of the selfish gene is the belief that the inheritance of acquired characters, or even phenotype in general, are not an evolutionary factor in any real physical sense. Genes are not naked in the world. They are usually packed together inside a genome, which is itself contained inside an organism. Sort of like microscopic interstellar travelers, genes build vehicles to promote their mutual interests of jumping into the next generation of vehicles.
Dawkin’s theories have had their opponents, including the evolutionary biologist Ernst Mayr (1904-2005):
Yet the funny thing is, that if you ask a man in the street who the greatest living Darwinian is, he will say Richard Dawkins. And indeed, Dawkins has done a marvelous job of popularizing Darwinism. But Dawkins’ basic theory of the gene being the object of evolution is totally non-Darwinian.
From Charles Darwin’s 1876 letter to Moritz Wagner:
In my opinion, the greatest error which I have committed, has not been allowing sufficient weight to the direct action of the environment, i.e. food, climate, etc., independently of natural selection.
Stephen Jay Gould (1941-2002) took issue with the gene as the unit of selection, arguing that genes are not directly “visible” to natural selection. 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. To Gould, gene differences do not cause evolutionary changes in populations; they register those changes.
Dawkins and his critics were united in assuming that genes are the only unit of heredity relevant to the evolution of organisms, and that acquired traits are not inherited, so it would be hard to consider the criticisms of the selfish gene concept as anything other than disagreements inside of an admittedly genocentric camp. Regarding the inheritance of behavior, the selfish gene hypothesis comes up rather short, a fact that Dawkins has himself acknowledged, promoting the idea of selfish genes instead as a “thought experiment” and as a “powerful and illuminating metaphor.”
Idea as Gene
One concept in The Selfish Gene I’ve always liked was Dawkins’ notion of a meme. For those who have never heard of the concept, at its simplest, a meme (rhymes with dream) is an idea. Any idea. It is simply something that gets stuck in the human mind.
Examples of memes are tunes, ideas, catch-phrases, clothes fashions, ways of making pots or of building arches. Just as genes propagate themselves in the gene pool by leaping from body to body via sperms or eggs, so memes propagate themselves in the meme pool by leaping from brain to brain via a process which, in the broad sense, can be called imitation. If a scientist hears, or reads about, a good idea, he passed it on to his colleagues and students. He mentions it in his articles and his lectures. If the idea catches on, it can be said to propagate itself, spreading from brain to brain.
You can think of a meme as a sort of ‘thought replicator’ stored in our human brains and passed on by the imitation of others. Some memes are helpful, others can be harmful. For example if you pulled up to a man on the side of the road that looked like a policemen, you might expect directions to a particular location to be accurate. However, people can simply walk into a uniform store and buy a policeman’s uniform. Some people may see a connection with memes to brain washing or thought manipulation, but that would not the case in anything but a tiny fraction. Most memes are passed along as a desire to inform, assist, or make a special statement about ourselves.
Our minds are not a blank slate on which any idea can be impressed. To be understood, a new meme must connect to the values and process that are already available to the individual. In addition one must also be willing to believe it or to take it serious. For example, although you are likely to understand the proposition that cartoon animals can talk with each other, you are unlikely to accept the proposition that this occurs in the real world without very strong evidence. Therefore, you will not add it to your ‘information base’ on animal characteristics. The cartoon meme will not manage to change your view on the subject.
Some writers think there are two basic types of memes: procedural and propagative. A good meme, like a good virus, will have special characteristics that insure continued growth. Without them, they eventually die.
- Fidelity: The ability to maintain accuracy and correct errors to maintain integrity.
- Fecundity: The fertility of the idea. The ease by which an idea it spawns itself. To me, this appears to be environmentally dependent. ‘Cultural relevance’ is probably a critical aspect of meme fecundity.
- Longevity: The longevity of an idea is related to how relevant it continues to be, as its meme is passed to newcomers and future generations.
- Co-adaption: Effective memes tend to thrive in the company of other replicators that compliment them.
Cancer as a Selfish Gene
What the selfish gene hypothesis does accomplish is provide an underpinning for the disturbing notion that genetic determinism can sometimes work at bewildering cross-purposes. The genes in an organism sometimes “disagree” over what should happen. That is, they appear to have opposing effects. For example, in some mammals, a gene in males may want to produce lots of healthy sperm, but others may want half the sperm to be defective. Some genes in a female may want her to nourish all her embryos; others might want her to abort half of them. Some genes in a fetus may want it to grow fast, others slowly, and yet at an intermediate rate. Some genes want to protect chromosomes from damage. Others want to damage it.
These conflicts arise because genes can spread into a population despite sometimes being harmful to the larger organism. These genes might give themselves a benefit but typically cause problems for other non-linked genes in the same creature. In that sense, they are indeed selfish. In fact we can define selfish genes by just such intent: stretches of DNA (genes, fragments, non-coding DNA, portions of chromosomes, whole chromosomes) that act narrowly to advance their own interests (replication) at the expense of the larger organism. This in turn leads to selection of other genes that try to suppress this activity, and thereby mitigate the harm. This evolution of selfish genetic elements and their relative control attempts inevitably leads to “intragenomic conflict.”
Most selfish genetic elements contrive to be transmitted as a disproportionate percentage into the organism’s progeny. Instead of being our idyllic, Mendelian 50%, selfish genes might manage to get into 66%, 99% or 50.01% of the organism’s progeny. Genes inherited in a biased manner can spread into a population without doing any good at all for the organism; it might even be harmful. Such a gene is said to “drive” or be “driven.”
Cancer is the ultimate intragenomic conflict, a selfish cell lineage. It is the inevitable results of the fact that cells within a multicellular organism are not quite genetically identical to each other, and become even less like each other over time, an effect that is inevitable, and is strongest in long-lived ones. Humans are genetic mosaics and within our bodies cell lineages can expand or contract according to their tendency to proliferate.
Cancers have evolved high rates of replication, compared with other cell clones, at the expense of host fitness. Precisely because cancers are harmful to the organism, there will be selection for properties of adaptations that can prevent or delay their occurrence. An indication of the importance of these adaptations can be seen when comparing adaptations in our own species to that of mice. Of the wild mice in the laboratory, raised under benign conditions, 46% will have gross tumors at death. Humans are 3000 times larger and live 20-30 times longer than mice, so if the probability of a cell becoming cancerous was the same per unit time in us as in mice, none of us would make it out of the womb alive, let alone reach puberty.
Portions excerpted from Fundamentals of Generative Medicine copyright 2010, Drum Hill Publishing, USA.