Is the selfish gene dead?
The Selfish Gene, by Richard Dawkins
David Dobbs recently suggested that the ‘selfish gene is one of the most successful science metaphors ever invented; unfortunately, it’s wrong.‘ He purports to uncover a scientific trend in genetics that trumps the understanding of the central role the gene plays in biological evolution. To parrot the author, unfortunately, he’s wrong. Dobbs describes the real phenomena of gene expression, and the fact that genes do not have to change for an organism to change its behavior, something that he refers to as genetic accommodation. He promotes the idea that gene expression is the engine of evolution rather than inheritable genes, without acknowledging that the variability of gene expression can only be preserved through inheritable genes, or that the concept of the selfish gene encapsulates this relationship between the two.
Multi-cellular organisms develop tissues as they mature. The cells that form a tissue express specific genes that provide structure or enzymes particular to the function of the tissue; these same cells inhibit expression of all other genes that code for functions performed by other tissues. This is simply the genetic explanation for tissue differentiation, and is an example of gene expression. This process is controlled by regulatory genes, and these genes are passed on to future offspring, allowing the same organism to perform the same functions in the same tissues generation after generation. Differential gene expression is ubiquitous, and regulatory genes that control gene expression are in fact the phenotypical result of genes themselves.
Genetic accommodation is a highly similar process: Gene expression driven by environmental stress, as in the author’s example, can create a worker, a drone or a queen bee; in another species, either a grasshopper or locust. This still requires genes to be turned on or off to stop expressing one set of genes and start expressing another, and such differential gene expression is again either controlled by other genes, or the genetic control includes some kind of environmental feedback. The function of environmental feedback in the control of gene expression has already been highly characterized. One of the earliest elucidations of this phenomenon is the lac operon, which is a set of related genes which control milk sugar metabolism. The lactase enzyme is constructed when milk sugar is present, because the milk sugar itself biochemically interacts with the gene control mechanism found in the lac operon to allow the lactase to be constructed; absence of milk sugar biochemically triggers inhibition of the same genes. In these gene expression mechanisms, any short-term response to the environment cannot be passed on to future individuals without changes to the genes coded in the germ cell DNA, in this example the genes for the lac operon, some of which are environmentally sensitive regulatory genes and one of which codes for the lactase enzyme.
Epigenetics is the study of gene expression controls outside of the DNA. Epigenetic control of gene expression is a recently established phenomenon, but inheritance of epigenetic changes across generations outside of the normal DNA replication mode is not. Again, epigenetic control of gene expression (via methylation mechanisms in control regions of DNA or on structural chromosomal histone proteins to help open unfold DNA to allow access for gene expression, or conversely to inhibit unfolding of DNA) itself requires biochemical reactions mediated by enzymes, coded for by . . . wait for it . . . DNA. There are some recent claims that epigenetic changes of somatic cells are being inherited by new generations, but that seems a huge stretch: Only germ cells create the DNA used to create new offspring, and there is no obvious mechanism that would propagate somatic changes to the germ cells. Arguing even more against this Lamarckian transformation is that during the replication of DNA for the construction of a germ cell, even the epigenetic markers on the chromosomes and the histones for the germ cells themselves are systematically removed. It is far more likely that any inheritance of epigenetic changes is in fact inheritance of germ cell DNA mutations or chromosomal rearrangements during meiosis of regulatory or control genes which epigenetically regulate or control the specific phenotype in the somatic tissue being observed.
For either epigenetics or genetic accommodation or other forms of gene expression to take the predominant role in evolution would first require that there be a demonstrated mechanism for passing these changes either outside of the well-defined DNA replication mode, or that these gene expressions somehow generated changes in the genes coded for in DNA such that they are passed on. The author presents no evidence or argument for an alternative mechanism.
There are other problems with the article; the only reason I bothered to comment on this article at all is that it addresses important recent discoveries and new understandings, but misunderstands or misconstrues their impact and how they fit into today’s biology. As it turns out, I found two other responses to this article which do a much clearer job of making my argument, this one by the evolutionary biologist Jerry Coyne: David Dobbs mucks up evolution, and this one, the response by the author of the Selfish Gene, Richard Dawkins: Adversarial journalism and the selfish gene.